Miracle-dz/UniFAR-FTUs huggingface dataset:
Fine-grained modularity and reuse of virtual machine components

Modularity is a key concept for large and complex applications and an important enabler for collaborative research. In comparison, virtual machines (VMs) are still mostly monolithic pieces of software. Our goal is to significantly reduce to the cost of extending VMs to efficiently host and execute multiple, dynamic languages. We are designing and implementing a VM following the "everything is extensible" paradigm. Among the novel use cases that will be enabled by our research are: VM extensions by third parties, support for multiple languages inside one VM, and a universal VM for mobile devices. Our research will be based on the existing state of the art. We will reuse an existing metacircular Java VM and an existing dynamic language VM implemented in Java. We will split the VMs into fine-grained modules, define explicit interfaces and extension points for the modules, and finally re-connect them. Performance is one of the most important concerns for VMs. Modularity improves flexibility but can introduce an unacceptable performance overhead at the module boundaries, e.g., for inter-module method calls. We will identify this overhead and address it with novel feedback-directed compiler optimizations. These optimizations will also improve the performance of modular applications running on top of our VM. The expected results of our research will be not only new insights and a new design approach for VMs, but also a complete reference implementation of a modular VM where everything is extensible by third parties and that supports multiple languages.
Jnk1 Deficiency in Hematopoietic Cells Suppresses Macrophage Apoptosis and Increases Atherosclerosis in Low-Density Lipoprotein Receptor Null Mice

Objective— The c-Jun NH2-terminal kinases (JNK) are regulated by a wide variety of cellular stresses and have been implicated in apoptotic signaling. Macrophages express 2 JNK isoforms, JNK1 and JNK2, which may have different effects on cell survival and atherosclerosis. Approach and Results— To dissect the effect of macrophage JNK1 and JNK2 on early atherosclerosis, Ldlr −/− mice were reconstituted with wild-type, Jnk1 −/−, and Jnk2 −/− hematopoietic cells and fed a high cholesterol diet. Jnk1 −/−→Ldlr −/− mice have larger atherosclerotic lesions with more macrophages and fewer apoptotic cells than mice transplanted with wild-type or Jnk2 −/− cells. Moreover, genetic ablation of JNK to a single allele (Jnk1 +/− /Jnk2 −/− or Jnk1 −/− /Jnk2 +/− ) in marrow of Ldlr −/− recipients further increased atherosclerosis compared with Jnk1 −/−→Ldlr −/− and wild-type→Ldlr −/− mice. In mouse macrophages, anisomycin-mediated JNK signaling antagonized Akt activity, and loss of Jnk1 gene obliterated this effect. Similarly, pharmacological inhibition of JNK1, but not JNK2, markedly reduced the antagonizing effect of JNK on Akt activity. Prolonged JNK signaling in the setting of endoplasmic reticulum stress gradually extinguished Akt and Bad activity in wild-type cells with markedly less effects in Jnk1 −/− macrophages, which were also more resistant to apoptosis. Consequently, anisomycin increased and JNK1 inhibitors suppressed endoplasmic reticulum stress–mediated apoptosis in macrophages. We also found that genetic and pharmacological inhibition of phosphatase and tensin homolog abolished the JNK-mediated effects on Akt activity, indicating that phosphatase and tensin homolog mediates crosstalk between these pathways. Conclusions— Loss of Jnk1, but not Jnk2, in macrophages protects them from apoptosis, increasing cell survival, and this accelerates early atherosclerosis.
HSP70 cleavage-induced photoreceptor cell death caused by N-methyl-N-nitrosourea

Retinal degenerative diseases (RDs) such as retinitis pigmentosa (RP) are characterized by slowly progressive photoreceptor cell death, but the molecular mechanism underlying RP remains unclear. Animal models for RP have led to a better understanding of the disease pathological mechanisms, yet it remains difficult to identify an appropriate genetic model for RDs in general because there are many causative genes (Rossmiller et al., 2012).
Persistence and involvement reconsidered: A phenomenology of African American college men who make a difference

The purpose of this study was to better understand how socially responsible leadership is experienced by African American men at a comprehensive university in the southeast. Employing the interpretive tradition of phenomenology, and building on college student retention, involvement, and leadership theories, the researcher asked 20 students what does making a difference mean and what is the result? Informants ascribed meanings to informal, individual encounters; but attributed outcomes to formal, group affiliations; and finally recommended formal, individual and community interventions. Furthermore, informants supported a non-positional, relational outlook on leadership and credited those relationships with persistence. Ultimately, the aim of phenomenology is to discover the essential structures of a lived experience. For these men, making a difference was structured by dialogue that developed a mindset to enable or enact positive role modeling and mentoring for other Black men. Thus, others are called to facilitate and further research cross cultural relationships that inspire student involvement.
Self-Reported Stickiness of Mind-Wandering Affects Task Performance

When asked to perform a certain task, we typically spend a decent amount of time thinking thoughts unrelated to that task–a phenomenon referred to as “mind-wandering. ” It is thought that this mind-wandering is driven at least in part by our unfinished goals and concerns. Previous studies have shown that just after presenting a participant with their own concerns, their reports of task-unrelated thinking increased somewhat. However, effects of these concerns on task performance were somewhat inconsistent. In this study we take the opposite approach, and examine whether task performance depends on the self-reported thought content. Specifically, a particularly intriguing aspect of mind-wandering that has hitherto received little attention is the difficulty of disengaging from it, in other words, the “stickiness” of the thoughts. While presenting participants with their own concerns was not associated with clear effects on task performance, we showed that the reports of off-task thinking and variability of response times increased with the amount of self-reported stickiness of thoughts. This suggests that the stickiness of mind-wandering is a relevant variable, and participants are able to meaningfully report on it.
Functional Genomic Analysis of Oligodendrocyte Differentiation

To better understand the molecular mechanisms governing oligodendrocyte (OL) differentiation, we have used gene profiling to quantitatively analyze gene expression in synchronously differentiating OLs generated from pure oligodendrocyte precursor cells in vitro. By comparing gene expression in these OLs to OLs generated in vivo, we discovered that the program of OL differentiation can progress normally in the absence of heterologous cell–cell interactions. In addition, we found that OL differentiation was unexpectedly prolonged and occurred in at least two sequential stages, each characterized by changes in distinct complements of transcription factors and myelin proteins. By disrupting the normal dynamic expression patterns of transcription factors regulated during OL differentiation, we demonstrated that these sequential stages of gene expression can be independently controlled. We also uncovered several genes previously uncharacterized in OLs that encode transmembrane, secreted, and cytoskeletal proteins that are as highly upregulated as myelin genes during OL differentiation. Last, by comparing genomic loci associated with inherited increased risk of multiple sclerosis (MS) to genes regulated during OL differentiation, we identified several new positional candidate genes that may contribute to MS susceptibility. These findings reveal a previously unexpected complexity to OL differentiation and suggest that an intrinsic program governs successive phases of OL differentiation as these cells extend and align their processes, ensheathe, and ultimately myelinate axons.
Sexuality, society, and feminism

This new volume challenges traditional perspectives into female sexuality and helps pave the way for revised understandings of women's sexuality. Top feminist scholars begin the task of molding conceptual models and methods of inquiry that will help shape a science for and about women. Taking the view that sexuality is socially constructed, the authors offer new insights into the epistemological data, theoretical models, and research methods on sexuality. At the book's core, the many issues central to how women discover the meaning of their sexuality in the world around them are explored. Topics discussed include the development of female sexuality at important points in the life-span, humor and sexuality, body image, sexual assertiveness, sexual harassment, and acquaintance rape. This readable and fascinating volume will provide an important starting point to carve out a feminist agenda for new scholarship in this too-long ignored part of women's lives.
ARABIDOPSIS : A RICH HARVEST 10 YEARS AFTER COMPLETION OF THE GENOME SEQUENCE Arabidopsis – a powerful model system for plant cell wall research

Aaron H. Liepman, Raymond Wightman, Naomi Geshi, Simon R. Turner and Henrik Vibe Scheller Biology Department, Eastern Michigan University, 316 Mark Jefferson Building, Ypsilanti, MI 48197, USA, Faculty of Life Science, University of Manchester, Oxford Road, Manchester M13 6AY, UK, VKR Research Centre, Department of Plant Biology and Biotechnology, University of Copenhagen, DK-1871 Frederiksberg C, Denmark, Feedstocks Division, Joint BioEnergy Institute, 5885 Hollis Street, Emeryville, CA 94608, USA, and Physical Biosciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
The safety and tolerability of GLP‐1 receptor agonists in the treatment of type 2 diabetes: a review

Although several classes of pharmacotherapy are available for type 2 diabetes, glycaemic control is often hampered by medication‐related adverse effects and contraindications such as renal impairment. Glucagon‐like peptide‐1 (GLP‐1) receptor agonists provide a new pharmacotherapeutic option based on the multiple glucose‐lowering effects of the human hormone GLP‐1. This mechanism of action not only provides therapeutic efficacy but also suggests that GLP‐1 receptor agonists have distinct safety and tolerability concerns compared with other diabetes therapies. Stimulation of pancreatic insulin secretion by GLP‐1 receptor agonists is glucose dependent, conferring a lesser risk of hypoglycaemia than that seen with sulfonylureas. Individual GLP‐1 receptor agonists differ in their metabolism and excretion profiles, affecting the choice of agent for patients with renal impairment. As with other protein‐based therapies, GLP‐1 receptor agonists may induce the formation of antibodies that may attenuate therapeutic efficacy and affect safety. Conclusions on cardiovascular safety must await outcomes studies, but at present no signal of harm has been reported, and preclinical data and effects on risk markers suggest a potential for benefit. Current data on thyroid medullary cancer in humans and pancreatic malignancy in rodents do not suggest that there is any reason to restrict the clinical use of GLP‐1 analogues in most people with diabetes. It is currently difficult to ascertain the possible contributory role of GLP‐1 receptor agonists in increasing the risk of pancreatitis, and vigilance for signs and symptoms is prudent. Primary tolerability issues include transient gastrointestinal symptoms, common with GLP‐1 receptor agonists, which can be reduced through dose titration. Copyright © 2011 John Wiley & Sons, Ltd.
Co-prescription of Gastro-protectants in Hospitalized Patients: An Analysis of What We Do and What We Think We Do

Background Proton pump inhibitors (PPIs) reduce the risk of upper gastrointestinal hemorrhage (UGIH) associated with the use of many medications. Goals To examine how clinicians perceive such risk and whether PPI coprescribing is based on an accurate assessment. Study Methods Clinicians in a single teaching hospital were asked to estimate risk of UGIH and comment on PPI coprescription in hypothetical patients. Records of 160 hospital in-patients (median age; 74 y) were then reviewed to examine PPI prescribing and risk factors for UGIH. Results In general, clinicians estimated UGIH risk accurately and reported low thresholds for PPI coprescription. Prescribing records showed regular PPI use increased between admission and discharge of patients from 61/160 (38%) to 93/160 (58%). Ten percent had a prior history of peptic ulcer disease. Proton pump inhibitor prescription was significantly associated with the use of aspirin and clopidogrel. Half of the patients with multiple risk factors for UGIH on admission and almost a third at discharge were not coprescribed a PPI. Conclusions Clinicians generally estimate correctly the risk of UGIH and report a low threshold for prescribing gastro-protection. Despite this, prescribing practice does not consistently take account of relative risk of UGIH. Targeted PPI coprescribing on the basis of risk factors would lead to more rational PPI use.
FGFR2 Gene Amplification in Gastric Cancer Predicts Sensitivity to the Selective FGFR Inhibitor AZD4547

Purpose: FGFR gene aberrations are associated with tumor growth and survival. We explored the role of FGFR2 amplification in gastric cancer and the therapeutic potential of AZD4547, a potent and selective ATP-competitive receptor tyrosine kinase inhibitor of fibroblast growth factor receptor (FGFR)1–3, in patients with FGFR2-amplified gastric cancer. Experimental Design: Array-comparative genomic hybridization and FISH were used to identify FGFR2 amplification in gastric cancer patient tumor samples. The effects of FGFR2 modulation were investigated in gastric cancer cells with FGFR2 amplification and in patient-derived gastric cancer xenograft (PDGCX) models using two approaches: inhibition with AZD4547 and short hairpin RNA (shRNA) knockdown of FGFR2. Results: Amplification of the FGFR2 gene was identified in a subset of Chinese and Caucasian patients with gastric cancer. Gastric cancer cell lines SNU-16 and KATOIII, carrying the amplified FGFR2 gene, were extremely sensitive to AZD4547 in vitro with GI50 values of 3 and 5 nmol/L, respectively. AZD4547 effectively inhibited phosphorylation of FGFR2 and its downstream signaling molecules and induced apoptosis in SNU-16 cells. Furthermore, inhibition of FGFR2 signaling by AZD4547 resulted in significant dose-dependent tumor growth inhibition in FGFR2-amplified xenograft (SNU-16) and PDGCX models (SGC083) but not in nonamplified models. shRNA knockdown of FGFR2 similarly inhibited tumor growth in vitro and in vivo. Finally, compared with monotherapy, we showed enhancement of in vivo antitumor efficacy using AZD4547 in combination with chemotherapeutic agents. Conclusion: FGFR2 pathway activation is required for driving growth and survival of gastric cancer carrying FGFR2 gene amplification both in vitro and in vivo. Our data support therapeutic intervention with FGFR inhibitors, such as AZD4547, in patients with gastric cancer carrying FGFR2 gene amplification. Clin Cancer Res; 19(9); 2572–83. ©2013 AACR.
Plausible Cooperation, Third Version

There is a large repeated games literature illustrating how future interactions provide incentives for cooperation. Much of the earlier literature assumes public monitoring: players always observe precisely the same thing. Departures from public monitoring to private monitoring that incorporate differences in players’ observations may dramatically complicate coordination and the provision of incentives, with the consequence that equilibria with private monitoring often seem unrealistically complex. We set out a model in which players accomplish cooperation in an intuitively plausible fashion. Players process information via a mental system — a set of psychological states and a transition function between states depending on observations. Players restrict attention to a relatively small set of simple strategies, and consequently, might learn which perform well.
Liposuction Normalizes – in Contrast to Other Therapies – Lymphedema-Induced Adipose Tissue Hypertrophy

Abstract The various types of treatment of lymphedema are under discussion and there has been some controversy regarding liposuction for lymphedema. Although it is clear that conservative therapies such as complex decongestive therapy (CDT) and controlled compression therapy (CCT) should be tried in the first instance, options for the treatment of late-stage lymphedema that is not responding to such treatment is not so clear. Improvements in technique, patient preparation, and patient follow-up have led to a greater and a wider acceptance of liposuction as a treatment for lymphedema. This paper outlines the benefits of using liposuction and presents the evidence to support its use.
Comparison of two compact 2D-FDFD methods and their application to extraction of circuit parameters

Compact 2D FDFD (two-dimensional finite- difference frequency-domain) methods were initially proposed by other researchers to solve the propagation constant of shielded uniform guided wave structures. In this paper, firstly we compare two compact 2D FDFD methods using four and six components of electromagnetic fields, which are applied to analyzing transmission lines with open boundaries. Then we extend them to extract the frequency-dependent circuit parameters of transmission lines. These R, L, C, G circuit parameters extracted via 1D transmission line theory are readily to be used for signal integrity analysis of high-speed circuits. I. INTRODUCTION High-speed effects of interconnect structures due to the increase in operating speed and decrease of the feature size in modern VLSI circuits, have to be carefully accounted for accurate signal integrity, power integrity and EMI/EMC analysis of modern circuit systems. The use of transmission line model becomes necessary in order to accurately capture the high-speed effects of interconnects. For the purpose of creating a proper transmission line model, very often the equivalent circuit parameters (R, L, C and G) need to be known in advance (1). This paper will focus on the compact 2D FDFD methods and apply them to extraction of circuit parameters. Characterization of transmission lines has been a topic of interest for many years, especially the analysis of the basic microstrip-like transmission line. Recently the compact two dimensional finite-difference frequency domain (2D FDFD) methods have been studied by several researchers (2-5) to analyze guided wave structures. Apart from its simple formulation, the advantage of 2D FDFD method is that we can obtain all the modes and modal field distribution of a uniform guided wave structure by solving an eigenvalue problem. The compact 2D FDFD method using four (3) and six (2, 5) field components have been proposed. In this paper, we will compare these two compact 2D FDFD methods used for analysis of guided wave structures. Then we will apply them to extract circuit parameters for the purpose of signal integrity analysis of high-speed circuit systems.
Lenition and Contrast: The Functional Consequences of Certain Phonetically Conditioned Sound Changes

This book analyzes 153 languages from a large variety of families to establish a previously unexplored relationship between phonetically conditioned sound changes such as lenitions and functional (meaning maintenance related) considerations. Carefully collecting numerous inventories of consonants, this collection is likely to become an important resource for future linguistics research. By distinguishing between phonetic and phonological neutralization, and showing that the first does not necessarily result in the second, Naomi Gurevich uncovers previously unexplored and often surprising trends in the relationship between phonetics and phonology.
A new algorithm for solving convex hull problem and its application to feature selection

A new method to solve the convex hull problem in n-dimensional spaces is proposed in this paper. At each step, a new point is added into the convex hull if the point is judged to be out of the current convex hull by a linear programming model. For the linear separable classification problem, if an instance is regarded as a point of the instances space, the overlap does not still occur between the convex hulls of different classes after a feature is deleted, then we can delete that feature. Repeat this process, an algorithm for feature selection is given. Experimental results show the effectiveness of the algorithm.
Separating the Anti-apoptotic and Mitotic Roles of Survivin*

Survivin is a bifunctional protein that acts as a suppressor of apoptosis and has an essential role in mitosis. To date whether these two functions can be divorced has not been addressed. Here we show that the linker region between the BIR (baculovirus inhibitor of apoptosis repeat) domain of survivin and COOH-terminal α helix may be the key to separating its roles. When overexpressed survivin is present in interphase cells and shuttles between the cytoplasm and nucleus. Here we identify a rev-like nuclear exportation signal (NES) in the central domain of survivin and demonstrate that point mutations within this region cause accumulation of survivin in the nucleus. Interestingly cells expressing NES mutants exhibit reduced survival after X-irradiation. Moreover, cells expressing survivinL98A-green fluorescent protein (GFP) showed increased poly(ADP-ribose) polymerase-cleavage and caspase-3 activity after tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) treatment compared with cells expressing full-length survivin-green fluorescent protein. These data suggest a direct link between the interphase localization of survivin and cellular responsiveness to apoptotic stimuli. Using a cell proliferation assay, we also found that ectopic expression of NES mutants can complement for depletion of endogenous survivin, indicating that they can execute the mitotic duties of survivin. Thus we demonstrate for the first time that 1) survivin has a functional NES; 2) nuclear accumulation of overexpressed survivin correlates with increased sensitivity of cells to ionising radiation; and 3) the anti-apoptotic and mitotic roles of survivin can be separated through mutation of its NES. Separating these two functions of survivin could open up new possibilities for therapeutic strategies aimed at eliminating cancer cells yet preserving normal cell viability.