Miracle-dz/UniFAR-FTUs huggingface dataset:
Cognitive and Motivational Characteristics of Adolescents Gifted in Mathematics: Comparisons Among Students With Different Types of Giftedness

Although numerous studies have compared cognitive and motivational characteristics between gifted versus nongifted students, research comparing those characteristics among different types of gifted students has not kept up with the theoretical development that saw a transition from unidimensional to multidimensional conceptualizations of giftedness. This study compares cognitive and motivational characteristics of high school students who are academically gifted in math, creatively talented in math, and nongifted. Whereas no differences were found among the three groups in their beliefs about ability, most of the other characteristics examined in the study distinguished the three groups. Academically gifted female students reported expending more effort than did academically gifted male students. Creatively talented males put forth more effort than academically gifted males, and the creatively talented in general used more cognitive strategies than the academically gifted. Overall, students who were either academically gifted or creatively talented in mathematics perceived that they were self-efficacious in general, used cognitive strategies, perceived their math ability and math self-efficacy to be high, and valued learning math more so than their nongifted age peers.
Atypical Neuroleptic Malignant Syndrome: Diagnostic Controversies and Considerations

Neuroleptic malignant syndrome (NMS) is a serious and potentially fatal adverse effect of antipsychotic drugs. The diagnosis of NMS commonly requires core symptoms of hyperthermia and muscle rigidity. Although diagnostic criteria for NMS have been established and are widely accepted and used, it should be recognized that atypical presentations pose a diagnostic dilemma, as hyperthermia and/or muscle rigidity may be absent or develop slowly over several days, leading to impairment or a significant delay in diagnosis and treatment. Evidence from case reports and retrospective evaluations supports a concept of atypical NMS, particularly with regard to treatment with atypical antipsychotics. However, it remains unclear whether these atypical presentations represent early or impending NMS. Furthermore, it is unclear whether dysfunction in other neurotransmitter systems, in addition to dopamine, may be involved in the pathogenesis of NMS induced by atypical antipsychotics. In patients receiving any antipsychotic, clinicians should carefully evaluate any features of NMS and should not prematurely exclude a diagnosis of NMS in cases where severe rigidity or hyperthermia is not initially apparent.
An Engineering Approach to Extending Lifespan in C. elegans

We have taken an engineering approach to extending the lifespan of Caenorhabditis elegans. Aging stands out as a complex trait, because events that occur in old animals are not under strong natural selection. As a result, lifespan can be lengthened rationally using bioengineering to modulate gene expression or to add exogenous components. Here, we engineered longer lifespan by expressing genes from zebrafish encoding molecular functions not normally present in worms. Additionally, we extended lifespan by increasing the activity of four endogenous worm aging pathways. Next, we used a modular approach to extend lifespan by combining components. Finally, we used cell- and worm-based assays to analyze changes in cell physiology and as a rapid means to evaluate whether multi-component transgenic lines were likely to have extended longevity. Using engineering to add novel functions and to tune endogenous functions provides a new framework for lifespan extension that goes beyond the constraints of the worm genome.
The Effect of Temperature on Anopheles Mosquito Population Dynamics and the Potential for Malaria Transmission

The parasites that cause malaria depend on Anopheles mosquitoes for transmission; because of this, mosquito population dynamics are a key determinant of malaria risk. Development and survival rates of both the Anopheles mosquitoes and the Plasmodium parasites that cause malaria depend on temperature, making this a potential driver of mosquito population dynamics and malaria transmission. We developed a temperature-dependent, stage-structured delayed differential equation model to better understand how climate determines risk. Including the full mosquito life cycle in the model reveals that the mosquito population abundance is more sensitive to temperature than previously thought because it is strongly influenced by the dynamics of the juvenile mosquito stages whose vital rates are also temperature-dependent. Additionally, the model predicts a peak in abundance of mosquitoes old enough to vector malaria at more accurate temperatures than previous models. Our results point to the importance of incorporating detailed vector biology into models for predicting the risk for vector borne diseases.
Ingroup Bias and Ingroup Projection in the Furry Fandom

In two studies, we examine ingroup favoritism within the furry community. Furry fans construct personas (“fursonas”) that are often related to a species of animal (e.g., fox, wolf). In Study 1, furries were found to rate their fursona species more favorably than other species. In Study 2, we examined whether the ingroup projection model may aid in understanding this ingroup species bias. Participants’ ratings of prototypicality of their species within the fandom was associated with greater favoritism of one’s species. A serial mediation model showed that identification with the fursona and perceived benefits of one’s fursona mediated the association between ingroup projection and ingroup species bias.
History Driven Program Repair

Effective automated program repair techniques have great potential to reduce the costs of debugging and maintenance. Previously proposed automated program repair (APR) techniques often follow a generate-and-validate and test-case-driven procedure: They first randomly generate a large pool of fix candidates and then exhaustively validate the quality of the candidates by testing them against existing or provided test suites. Unfortunately, many real-world bugs cannot be repaired by existing techniques even after more than 12 hours of computation in a multi-core cloud environment. More work is needed to advance the capabilities of modern APR techniques. We propose a new technique that utilizes the wealth of bug fixesacross projects in their development history to effectively guide and drive a programrepair process. Our main insight is that recurring bug fixes are common inreal-world applications, and that previously-appearing fix patterns canprovide useful guidance to an automated repair technique. Based on this insight, our technique first automaticallymines bug fix patterns from the history of many projects. We then employ existingmutation operators to generate fix candidates for a given buggy program. Candidates that match frequently occurring historical bug fixes are consideredmore likely to be relevant, and we thus give them priority inthe random search process. Finally, candidates thatpass all the previously failed test cases are recommended as likely fixes. We compare our technique against existinggenerate-and-validate and test-driven APR approaches using 90 bugs from 5 Javaprograms. The experiment results show that our technique can producegood-quality fixes for many more bugs as compared to the baselines, while beingreasonably computationally efficient: it takes less than 20minutes, on average, to correctly fix a bug.
Covariant vortex in superconducting-superfluid-normal fluid mixtures with a stiff equation of state

Using a covariant description, we obtain the integrals of motion for a cylindrically symmetric, stationary vortex configuration in a mixture of interacting superconductors, superfluids and normal fluids. We then integrate the stress-energy density and find a very simple, closed expression for the energy per unit length and the relevant stress coefficients of the vortex with respect to a vortex-free reference state. This result is found assuming a ‘‘stiff’’ equation of state for the fluid mixture, which is the least compressible but still causal equation of state ~contrary to the incompressible case! As an illustration for these general results, we discuss some applications to ‘‘real’’ superfluid-superconducting systems that are contained as special cases. These include the two-fluid model for He-II, uncharged binary superfluid mixtures, conventional superconductors and the superfluid neutron-proton-electron plasma in the outer core of neutron stars. The subject of investigation in the present work is the structure and energy of a stationary and cylindrically symmetric quantized vortex in an interacting multi-fluid mixture, which may consist of charged and uncharged superfluids and of normal fluids. This analysis has initially been motivated by the superfluid mixture commonly found in neutron star models, namely in the outer core region, where superfluid neutrons, superconducting protons and normal electrons are generally thought to coexist. However, because of the generality of the present approach, it is equally well applicable to superfluid and superconducting systems found in more common laboratory contexts, some of which will be discussed briefly in the concluding Sec. VIII.
Iterative multiuser detection for CDMA with FEC: near-single-user performance

This paper introduces an iterative multiuser receiver for direct sequence code-division multiple access (DS-CDMA) with forward error control (FEC) coding. The receiver is derived from the maximum a posteriori (MAP) criterion for the joint received signal, but uses only single-user decoders. Iterations of the system are used to improve performance, with dramatic effects. Single-user turbo code decoders are utilized as the FEC system and a complexity study is presented. Simulation results show that the performance approaches single-user performance even for moderate signal-to-noise ratios.
SAOS-2 Osteosarcoma Cells Bind Fibroblasts via ICAM-1 and This Is Increased by Tumour Necrosis Factor-α

We recently reported exchange of membrane and cytoplasmic markers between SAOS-2 osteosarcoma cells and human gingival fibroblasts (h-GF) without comparable exchange of nuclear markers, while similar h-GF exchange was seen for melanoma and ovarian carcinoma cells. This process of “cellular sipping” changes phenotype such that cells sharing markers of both SAOS-2 and h-GF have morphology intermediate to that of either cell population cultured alone, evidencing increased tumour cell diversity without genetic change. TNF-α increases cellular sipping between h-GF and SAOS-2, and we here study binding of SAOS-2 to TNF-α treated h-GF to determine if increased cellular sipping can be accounted for by cytokine stimulated SAOS-2 binding. More SAOS-2 bound h-GF pe-seeded wells than culture plastic alone (p<0.001), and this was increased by h-GF pre-treatment with TNF-α (p<0.001). TNF-α stimulated binding was dose dependent and maximal at 1.16nM (p<0.05) with no activity below 0.006 nM. SAOS-2 binding to h-GF was independent of serum, while the lipopolysaccharide antagonist Polymyxin B did not affect results, and TNF-α activity was lost on boiling. h-GF binding of SAOS-2 started to increase after 30min TNF-α stimulation and was maximal by 1.5hr pre-treatment (p<0.001). h-GF retained maximal binding up to 6hrs after TNF-α stimulation, but this was lost by 18hrs (p<0.001). FACS analysis demonstrated increased ICAM-1 consistent with the time course of SAOS-2 binding, while antibody against ICAM-1 inhibited SAOS-2 adhesion (p<0.04). Pre-treating SAOS-2 with TNF-α reduced h-GF binding to background levels (p<0.003), and this opposite effect to h-GF cytokine stimulation suggests that the history of cytokine exposure of malignant cells migrating across different microenvironments can influence subsequent interactions with fibroblasts. Since cytokine stimulated binding was comparable in magnitude to earlier reported TNF-α stimulated cellular sipping, we conclude that TNF-α stimulated cellular sipping likely reflects increased SAOS-2 binding as opposed to enhanced exchange mechanisms.
Synergistic Blockade of EGFR and HER2 by New-Generation EGFR Tyrosine Kinase Inhibitor Enhances Radiation Effect in Bladder Cancer Cells

Blockade of EGFR has been proved useful in enhancing the effect of radiotherapy, but the advantages of new-generation EGFR tyrosine kinase inhibitors (TKI) in radiosensitization are not well known. We used two human bladder cancer cells with wild-type EGFR to study the synergism between irradiation and afatinib (an EGFR/HER2 dual kinase inhibitor) or erlotinib (an EGFR kinase inhibitor). Here, we showed that afatinib has better radiosensitizing effect than erlotinib in increasing cancer cell killing, the percentage of apoptotic cells, and DNA damage. Afatinib is also superior to erlotinib in combining radiation to decrease tumor size, inhibit glucose metabolism, and enhance apoptotic proteins in vivo. Finally, erlotinib suppressed cell growth and induced more DNA damage in bladder cancer cells transfected with HER2 shRNA, but not in control vector-treated cells. In conclusion, concomitant blockade of radiation-activated EGFR and HER2 signaling by a new-generation EGFR TKI better inhibits the growth of bladder cancer cells both in vitro and in vivo. The absence of radiosensitization by EGFR inhibition alone and the greater radiosensitizing effect of EGFR inhibitor in HER2 knocked down cells suggest the synergism between HER2 and EGFR in determining radiosensitivity. The regained radiosensitizing activity of erlotinib implies that with proper HER2 inhibition, EGFR tyrosine kinase is still a potential target to enhance radiotherapy effect in these seemingly unresponsive bladder cancer cells. Mol Cancer Ther; 14(3); 810–20. ©2015 AACR.
Platelet/Endothelial Biomarkers in Depressed Patients Treated With the Selective Serotonin Reuptake Inhibitor Sertraline After Acute Coronary Events: The Sertraline AntiDepressant Heart Attack Randomized Trial (SADHART) Platelet Substudy

Background—Depression after acute coronary syndromes (ACSs) has been identified as an independent risk factor for subsequent cardiac death. Enhanced platelet activation has been hypothesized to represent 1 of the mechanisms underlying this association. Selective serotonin reuptake inhibitors (SSRIs) are known to inhibit platelet activity. Whether treatment of depressed post-ACS patients with SSRIs alters platelet function was not known. Accordingly, we serially assessed the release of established platelet/endothelial biomarkers in patients treated with sertraline vs placebo in the Sertraline AntiDepressant Heart Attack Randomized Trial (SADHART). Methods and Results—Plasma samples (baseline, week 6, and week 16) were collected from patients randomized to sertraline (n=28) or placebo (n=36). Anticoagulants, aspirin, and ADP-receptor inhibitors were permitted in this study. Platelet factor 4, &bgr;-thromboglobulin (&bgr;TG), platelet/endothelial cell adhesion molecule-1, P-selectin, thromboxane B2, 6-ketoprostaglandin F1a, vascular cell adhesion molecule-1, and E-selectin were measured by ELISA. Treatment with sertraline was associated with substantially less release of platelet/endothelial biomarkers than was treatment with placebo. These differences attained statistical significance for &bgr;TG (P =0.03) at weeks 6 and 16 and for P-selectin (P =0.04) at week 16. Repeated-measures ANOVA revealed a significant advantage for sertraline vs placebo for diminishing E-selectin and &bgr;TG concentrations across the entire treatment period. Conclusions—Treatment with sertraline in depressed post-ACS patients is associated with reductions in platelet/endothelial activation despite coadministration of widespread antiplatelet regimens including aspirin and clopidogrel. The antiplatelet and endothelium-protective properties of SSRIs might represent an attractive additional advantage in patients with depression and comorbid coronary artery and/or cerebrovascular disease.
Does Bone Morphogenetic Protein 6 (BMP6) Affect Female Fertility in the Mouse?1

Bone morphogenetic protein 6 (BMP6) is a transforming growth factor beta superfamily member produced by mammalian oocytes as well as other cell types. Despite well-characterized effects of recombinant BMP6 on granulosa cells in vitro, the function of BMP6 in vivo has been ill-defined. Therefore, the effects of genetic deletion of the Bmp6 gene on female mouse fertility were assessed. The mean litter size of Bmp6−/− females was reduced by 22% (P < 0.05) compared to Bmp6+/+ controls. Not only did Bmp6−/− females naturally ovulate 24% fewer eggs, but competence of in vitro-matured oocytes to complete preimplantation development after fertilization in vitro was decreased by 50%. No apparent effect of Bmp6 deletion on either the morphology or the dynamics of follicular development was apparent. Nevertheless, levels of luteinizing hormone (LH)/human chorionic gonadotropin (hCG)-induced transcripts, which encode proteins required for cumulus expansion (HAS2, PTGS2, PTX3, and TNFAIP6), and of epidermal growth factor-like peptides (AREG, BTC, and EREG) were lower in Bmp6−/− mice than in controls after administration of a reduced dose of hCG (1 IU) in vivo. LH receptor (Lhcgr) transcript levels were not significantly lower in Bmp6−/− granulosa cells, suggesting that BMP6 is required for processes downstream of LH receptors. To assess whether another oocyte-derived BMP, BMP15, could have BMP6-redundant functions in vivo, the fertility of Bmp15/Bmp6 double mutants was assessed. Fertility was not significantly reduced in double-homozygous mutants compared with that in double-heterozygous controls. Therefore, BMP6 promotes normal fertility in female mice, at least in part, by enabling appropriate responses to LH and normal oocyte quality. Thus, Bmp6 probably is part of the complex genetic network that determines female fertility.
Changes in beta 2-adrenoceptor and other signaling proteins produced by chronic administration of 'beta-blockers' in a murine asthma model.

BACKGROUND We have previously reported that chronic treatment with certain 'beta-blockers' reduces airway hyperresponsiveness (AHR) to methacholine in a murine model of asthma. METHODS Airway resistance was measured using the forced oscillation technique in ovalbulmin-sensitized and ovalbulmin-challenged mice treated with several beta-adrenoceptor (beta-AR) ligands. We used the selective beta 2-AR ligand ICI 118,551 and the preferential beta 1-AR ligand metoprolol to investigate the receptor subtype mediating the beneficial effect. Expression of beta-ARs was evaluated using immunofluorescence. We evaluated several signaling proteins by western blot using lung homogenates, and measured the relaxation of the isolated trachea produced by EP2 and IP receptor agonists. RESULTS Four findings were associated with the decreased AHR after chronic beta-blocker treatment: (1) the highly selective beta 2-AR antagonist/inverse agonist, ICI 118,551 produced the bronchoprotective effect; (2) beta 2-AR up-regulation resulted from chronic 'beta-blocker' treatment; (3) reduced expression of certain proteins involved in regulating bronchial tone, namely, Gi, phosphodiesterase 4D and phospholipase C-beta 1; and (4) an enhanced bronchodilatory response to prostanoid agonists for the IP and EP2 receptors. CONCLUSIONS These data suggest that in the murine model of asthma, several compensatory changes associated with either increased bronchodilator signaling or decreased bronchoconstrictive signaling, result from the chronic administration of certain 'beta-blockers'.
Does Motivation Matter When Assessing Trade Performance? An Analysis of Mutual Funds

We relate the performance of mutual fund trades to their motivation. A fund manager who buys stocks when there are heavy investor outflows is likely to be motivated by the belief that the stocks are significantly undervalued. In contrast, when there are heavy inflows, the manager is likely to be motivated to work off excess liquidity by buying stocks. Our analysis reveals that managers making purely valuation-motivated purchases substantially beat the market but are unable to do so when compelled to invest excess cash from investor inflows. A similar, but weaker, pattern is found for stocks that are sold. (JEL G11, G29) Copyright 2007, Oxford University Press.
Group Consensus and Psychological Well‐Being: A Large Field Study1

Models of group process propose that stressful social environments develop when there is a lack of consensus among group members about issues of relevance to the group. Based on these models, we expected that levels of consensus would be positively related to the average levels of psychological well-being in naturally occurring work groups. An examination of data from 3,546 respondents within 73 work groups revealed that levels of consensus about leadership and peer relations were positively related to the average psychological well-being of the group members, even after controlling for absolute level effects and covariates. In contrast, levels of consensus were not related to the average psychological well-being of group members when identical analyses were conducted using pseudogroups.
Mitotic Defects Lead to Pervasive Aneuploidy and Accompany Loss of RB1 Activity in Mouse LmnaDhe Dermal Fibroblasts

Background Lamin A (LMNA) is a component of the nuclear lamina and is mutated in several human diseases, including Emery-Dreifuss muscular dystrophy (EDMD; OMIM ID# 181350) and the premature aging syndrome Hutchinson-Gilford progeria syndrome (HGPS; OMIM ID# 176670). Cells from progeria patients exhibit cell cycle defects in both interphase and mitosis. Mouse models with loss of LMNA function have reduced Retinoblastoma protein (RB1) activity, leading to aberrant cell cycle control in interphase, but how mitosis is affected by LMNA is not well understood. Results We examined the cell cycle and structural phenotypes of cells from mice with the Lmna allele, Disheveled hair and ears (LmnaDhe). We found that dermal fibroblasts from heterozygous LmnaDhe (LmnaDhe/+) mice exhibit many phenotypes of human laminopathy cells. These include severe perturbations to the nuclear shape and lamina, increased DNA damage, and slow growth rates due to mitotic delay. Interestingly, LmnaDhe/+ fibroblasts also had reduced levels of hypophosphorylated RB1 and the non-SMC condensin II-subunit D3 (NCAP-D3), a mitosis specific centromere condensin subunit that depends on RB1 activity. Mitotic check point control by mitotic arrest deficient-like 1 (MAD2L1) also was perturbed in LmnaDhe /+ cells. LmnaDhe /+ fibroblasts were consistently aneuploid and had higher levels of micronuclei and anaphase bridges than normal fibroblasts, consistent with chromosome segregation defects. Conclusions These data indicate that RB1 may be a key regulator of cellular phenotype in laminopathy-related cells, and suggest that the effects of LMNA on RB1 include both interphase and mitotic cell cycle control.
Galois module structure of Galois cohomology for embeddable cyclic extensions of degree pn

Let p > 2 be prime and let n, m ∈ ℕ be given. For cyclic extensions E/F of degree pn that contain a primitive pth root of unity, we show that the associated 𝔽p[Gal(E/F)]‐modules Hm(GE, μp) have a sparse decomposition. When E/F is additionally a subextension of a cyclic, degree pn+1 extension E′/F, we give a more refined 𝔽p[Gal(E/F)]‐decomposition of Hm(GE, μp).