Miracle-dz/UniFAR-FTUs huggingface dataset:
Personal Values and Intergroup Empathy

Empirical evidence shows that personal values have an influence on empathy in intrapersonal relationships. We examine the relationship between the values of self-enhancement and self-transcendence among members of the majority group (Israeli Jews) and empathy towards in-group and out-group members (Israeli Arabs). Two hundred and ninety-seven Israeli Jewish students took part in the study. While the results show that self-transcendence values have a consistent effect on empathy whether it is towards in-group or out-group members, the hypotheses regarding the impact of self-enhancement values on empathy towards out-group members were partly supported. We discuss the universality of self-transcendence values in their influence on empathy in different contexts and emphasize the complex relationships among in-group members.
Factors influencing relapse in schizophrenia: A longitudinal study in China

Identifying predictors of relapse in Schizophrenia (SZ) has been a hot issue since relapse is associated with worse clinical outcome. In this study, relapse rates of SZ patients after hospital discharge and their possible factors were investigated annually over 3 years to differentiate short-term and long-term predictors for relapse in SZ in China. According to the sequence of discharge date, 420 SZ patients were recruited. The severity of disease, compliance with medication use, social functions, and relapse rate were assessed at the time points of 1-, 2- and 3-year after hospital discharge. After each assessment, only the not-relapsed participants remained in the study for the next assessment. The factors influencing relapse in SZ were analysed by a logistic regression. Our results indicated that the relapse rate at 1-, 2- and 3-year after hospital discharge was 33.0%, 29.8%, and 16.4%, respectively. Compliance with medication use, communication skills, and work/study functioning were associated with relapse in SZ, with differential long-term and short-term effects. Especially, the compliance with medication use in the relapsed participants were significantly worse than that in the not-relapsed participants in three assessments over 3 years (P<0.001). Logistic regression analyses also revealed that SZ patients with worse compliance with medication use, communication skills, and work/study functioning showed higher risk of relapse. Importantly, worse compliance with medication use was associated with a 6.369-, 13.889-, and 8.850- fold increase in relapse at 1-, 2- and 3-year after hospital discharge, respectively (P<0.001). To our knowledge, this is the first longitudinal study to investigate factors influencing relapse in SZ in China. Our results demonstrated that good compliance with medication use, communication skills, and work/study functioning may reduce the risk of relapse in SZ. The findings of this study suggested that good compliance with medication use is critical to prevention of SZ relapse.
Prospective study of ultraviolet radiation exposure and risk of cancer in the United States

Ecologic studies have reported that solar ultraviolet radiation (UVR) exposure is associated with cancer; however, little evidence is available from prospective studies. We aimed to assess the association between an objective measure of ambient UVR exposure and risk of total and site‐specific cancer in a large, regionally diverse cohort [450,934 white, non‐Hispanic subjects (50–71 years) in the prospective National Institutes of Health (NIH)‐AARP Diet and Health Study] after accounting for individual‐level confounding risk factors. Estimated erythemal UVR exposure from satellite Total Ozone Mapping Spectrometer (TOMS) data from NASA was linked to the US Census Bureau 2000 census tract (centroid) of baseline residence for each subject. We used Cox proportional hazards models adjusted for multiple potential confounders to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for quartiles of UVR exposure. Restricted cubic splines examined nonlinear relationships. Over 9 years of follow‐up, UVR exposure was inversely associated with total cancer risk (N = 75,917; highest versus lowest quartile; HR = 0.97, 95% CI = 0.95–0.99; p‐trend < 0.001). In site‐specific cancer analyses, UVR exposure was associated with increased melanoma risk (highest versus lowest quartile; HR = 1.22, 95% CI = 1.13–1.32; p‐trend < 0.001) and decreased risk of non‐Hodgkin's lymphoma (HR = 0.82, 95% CI = 0.74–0.92) and colon (HR = 0.88, 95% CI = 0.82–0.96), squamous cell lung (HR = 0.86, 95% CI = 0.75–0.98), pleural (HR = 0.57, 95% CI = 0.38–0.84), prostate (HR = 0.91, 95% CI = 0.88–0.95), kidney (HR = 0.83, 95% CI = 0.73–0.94) and bladder (HR = 0.88, 95% CI = 0.81–0.96) cancers (all p‐trend < 0.05). We also found nonlinear associations for some cancer sites, including the thyroid and pancreas. Our results add to mounting evidence for the influential role of UVR exposure on cancer.
The Concentrations of EGFR, LRG1, ITIH4, and F5 in Serum Correlate with the Number of Colonic Adenomas in ApcPirc/+ Rats

The development of noninvasive methods for early detection of colon cancer is critical for the successful management of this disease. Using a targeted quantitative proteomics technique, we assessed the ability of 12 serum proteins to detect the presence of colonic polyps in the ApcPirc/+ rat model of familial colon cancer. Serum protein candidates were selected from gene transcripts upregulated in colonic tumors of ApcPirc/+ rats and from a prior study of serum proteins differentially expressed in mice carrying intestinal adenomas. Proteins were quantified at early stages of polyp formation in a rat cohort monitored longitudinally by colonoscopy over a period of 75 days. Of the 12 proteins monitored at three distinct time points, seven showed differential expression in at least one time point in the serum from ApcPirc/+ rats compared with wild-type rats. Tumor multiplicity correlated with protein expression changes, and most tumors grew during the study. EGFR, LRG1, ITIH4, and F5 displayed the most robust tumor-associated protein expression changes over time. Receiver operator characteristic analysis using these four proteins resulted in a sensitivity of 100%, a specificity of 80%, and an area under the curve of 0.93 at 135 days of age, when the Pirc rats bore an average of 19 tumors in the colon and seven in the small intestine. The results of this study demonstrate that the quantitative analysis of a panel of serum proteins can detect the presence of early intestinal tumors in a rat model, and provides support for future measurements in humans. Cancer Prev Res; 7(11); 1160–9. ©2014 AACR.
Degenerate Recognition of MHC Class I Molecules with Bw4 and Bw6 Motifs by a Killer Cell Ig-like Receptor 3DL Expressed by Macaque NK Cells

The killer cell Ig-like receptors (KIRs) expressed on the surface of NK cells recognize specific MHC class I (MHC-I) molecules and regulate NK cell activities against pathogen-infected cells and neoplasia. In HIV infection, survival is linked to host KIR and MHC-I genotypes. In the SIV macaque model, however, the role of NK cells is unclear due to the lack of information on KIR–MHC interactions. In this study, we describe, to our knowledge, the first in-depth characterization of KIR–MHC interactions in pigtailed macaques (Macaca nemestrina). Initially, we identified three distinct subsets of macaque NK cells that stained ex vivo with macaque MHC-I tetramers loaded with SIV peptides. We then cloned cDNAs corresponding to 15 distinct KIR3D alleles. One of these, KIR049-4, was an inhibitory KIR3DL that bound MHC-I tetramers and prevented activation, degranulation, and cytokine production by macaque NK cells after engagement with specific MHC-I molecules on the surface of target cells. Furthermore, KIR049-4 recognized a broad range of MHC-I molecules carrying not only the Bw4 motif, but also Bw6 and non-Bw4/Bw6 motifs. This degenerate, yet peptide-dependent, MHC reactivity differs markedly from the fine specificity of human KIRs.
Stereospecific Metabolism of R- and S-Warfarin by Human Hepatic Cytosolic Reductases

Coumadin (rac-warfarin) is the most commonly used anticoagulant in the world; however, its clinical use is often challenging because of its narrow therapeutic range and interindividual variations in response. A critical contributor to the uncertainty is variability in warfarin metabolism, which includes mostly oxidative but also reductive pathways. Reduction of each warfarin enantiomer yields two warfarin alcohol isomers, and the corresponding four alcohols retain varying levels of anticoagulant activity. Studies on the kinetics of warfarin reduction have often lacked resolution of parent-drug enantiomers and have suffered from coelution of pairs of alcohol metabolites; thus, those studies have not established the importance of individual stereospecific reductive pathways. We report the first steady-state analysis of R- and S-warfarin reduction in vitro by pooled human liver cytosol. As determined by authentic standards, the major metabolites were 9R,11S-warfarin alcohol for R-warfarin and 9S,11S-warfarin alcohol for S-warfarin. R-warfarin (Vmax 150 pmol/mg per minute, Km 0.67 mM) was reduced more efficiently than S-warfarin (Vmax 27 pmol/mg per minute, Km 1.7 mM). Based on inhibitor phenotyping, carbonyl reductase-1 dominated R-and S-warfarin reduction, followed by aldo-keto reductase-1C3 and then other members of that family. Overall, the carbonyl at position 11 undergoes stereospecific reduction by multiple enzymes to form the S alcohol for both drug enantiomers, yet R-warfarin undergoes reduction preferentially. This knowledge will aid in assessing the relative importance of reductive pathways for R- and S-warfarin and factors influencing levels of pharmacologically active parent drugs and metabolites, thus impacting patient dose responses.
Scalable and Efficient Flow-Based Community Detection for Large-Scale Graph Analysis

Community detection is an increasingly popular approach to uncover important structures in large networks. Flow-based community detection methods rely on communication patterns of the network rather than structural properties to determine communities. The Infomap algorithm in particular optimizes a novel objective function called the map equation and has been shown to outperform other approaches in third-party benchmarks. However, Infomap and its variants are inherently sequential, limiting their use for large-scale graphs. In this article, we propose a novel algorithm to optimize the map equation called RelaxMap. RelaxMap provides two important improvements over Infomap: parallelization, so that the map equation can be optimized over much larger graphs, and prioritization, so that the most important work occurs first, iterations take less time, and the algorithm converges faster. We implement these techniques using OpenMP on shared-memory multicore systems, and evaluate our approach on a variety of graphs from standard graph clustering benchmarks as well as real graph datasets. Our evaluation shows that both techniques are effective: RelaxMap achieves 70% parallel efficiency on eight cores, and prioritization improves algorithm performance by an additional 20--50% on average, depending on the graph properties. Additionally, RelaxMap converges in the similar number of iterations and provides solutions of equivalent quality as the serial Infomap implementation.
Epigenetics of Nicotine: Another Nail in the Coughing

Chronic nicotine exposure rewired the brains of rodents and enhanced their behavioral response to cocaine. In a mouse model, chronic nicotine exposure before cocaine use exacerbated the epigenetic, gene-expression, electrophysiological, and behavioral effects that occur during the transition from acute to chronic responses to cocaine that have been linked with the addictive process. Nicotine enhancement of the effects can be mimicked with an inhibitor of chromatin-modifying enzymes (class I and II histone deacetylases). These findings may spur the discovery of therapeutics for the treatment of addiction.
The Pharmacology of Autonomic Failure: From Hypotension to Hypertension

Primary neurodegenerative autonomic disorders are characterized clinically by loss of autonomic regulation of blood pressure. The clinical picture is dominated by orthostatic hypotension, but supine hypertension is also a significant problem. Autonomic failure can result from impairment of central autonomic pathways (multiple system atrophy) or neurodegeneration of peripheral postganglionic autonomic fibers (pure autonomic failure, Parkinson’s disease). Pharmacologic probes such as the ganglionic blocker trimethaphan can help us in the understanding of the underlying pathophysiology and diagnosis of these disorders. Conversely, understanding the pathophysiology is crucial in the development of effective pharmacotherapy for these patients. Autonomic failure patients provide us with an unfortunate but unique research model characterized by loss of baroreflex buffering. This greatly magnifies the effect of stimuli that would not be apparent in normal subjects. An example of this is the discovery of the osmopressor reflex: ingestion of water increases blood pressure by 30–40 mm Hg in autonomic failure patients. Animal studies indicate that the trigger of this reflex is related to hypo-osmolality in the portal circulation involving transient receptor potential vanilloid 4 receptors. Studies in autonomic failure patients have also revealed that angiotensin II can be generated through noncanonical pathways independent of plasma renin activity to contribute to hypertension. Similarly, the mineralocorticoid receptor antagonist eplerenone produces acute hypotensive effects, highlighting the presence of non-nuclear mineralocorticoid receptor pathways. These are examples of careful clinical research that integrates pathophysiology and pharmacology to advance our knowledge of human disease.
Lessons from Australia: Human Papillomavirus Is Not a Major Risk Factor for Esophageal Squamous Cell Carcinoma

The incidence of esophageal cancer exhibits great geographic diversity, with up to 20-fold differences in rates between high- and low-risk areas ([1][1]). Despite stable or even declining worldwide esophageal cancer rates over the last few decades ([2][2], [3][3]), this disease remains a substantial
Selective expression of liver and activation‐regulated chemokine (LARC) in intestinal epithelium in mice and humans

The liver and activation‐regulated chemokine (LARC), also termed MIP‐3α and Exodus, is a novel human CC chemokine with a selective chemotactic activity for lymphocytes and dendritic cells. Here we describe genomic and cDNA clones encoding the murine orthologue of LARC (mLARC). The gene consists of four exons and three introns. The 5′‐noncoding region of about 400 bp contains typical TATA and CAAT boxes but no other potential regulatory elements so far described. The cDNA encodes a CC chemokine of 97 amino acid residues with the highest homology to human LARC (64 % amino acid identity). The 3′‐noncoding region contains as many as five potential mRNA destabilization signals. mLARC was strongly and transiently induced in the murine monocytoid cell line J774 by lipopolysaccharide (LPS) but not by cytokines such as TNF‐α, IFN‐γ, IL‐1β or IL‐4. In normal mice, mLARC mRNA was expressed selectively in intestinal tissues such as small intestine and colon. Upon treatment with LPS, mLARC expression was enhanced in intestinal tissues and induced in some lymphoid tissues such as lymph nodes. Because of alternative splicing, there are two types of transcripts encoding mLARC and its variant mLARCvar with and without an N‐terminal alanine in the mature protein, respectively. Both types of transcripts appeared to be expressed in various mouse tissues. In situ hybridization revealed that epithelial cells of intestinal tissues, especially those lining lymphoid follicles, expressed mLARC. Localization of LARC mRNA in epithelial cells was also demonstrated in a human appendix. Furthermore, mLARC was efficiently chemotactic for cells such as γ δ type T cells in intestinal epithelium and naive B cells in Peyer's patches. Thus, in both humans and mice, LARC may be physiologically involved in formation and function of the mucosal lymphoid tissues by attracting lymphocytes and dendritic cells toward epithelial cells.
Identifying the Interaction Between Influenza and Pneumococcal Pneumonia Using Incidence Data

Influenza virus increases susceptibility to pneumococcal pneumonia in individuals but has only a modest impact on the total population. Tipping the Scales for Pathogen Interaction As if it weren’t bad enough to be infected by one pathogen, sometimes a primary infection can pave the way for a secondary infection as well. This has been thought to be the case with influenza virus and Streptococcus pneumoniae. Indeed, there are a lot of data in both humans and animal models that this does happen at the individual level. However, epidemiological studies measuring population-level effects do not reflect this observation. Now, Shrestha et al. use mathematical modeling of weekly incidence reports to reconcile these two seemingly disparate observations. The authors constructed a mechanistic transmission model within a likelihood-based inference framework and characterized the timing, nature, and magnitude of the interaction between influenza virus and pneumococcal pneumonia. In individuals, they see that flu increases the susceptibility to subsequent pneumococcal pneumonia more than 100 times. However, at the population level, there is only a modest effect. These data suggest that influenza virus may contribute to pneumococcal pneumonia pathogenesis, but that these effects may be masked in the total population. The association between influenza virus and the bacterium Streptococcus pneumoniae (pneumococcus) has been proposed as a polymicrobial system, whereby transmission and pathogenicity of one pathogen (the bacterium) are affected by interactions with the other (the virus). However, studies focusing on different scales of resolution have painted an inconsistent picture: Individual-scale animal experiments have unequivocally demonstrated an association, whereas epidemiological support in human populations is, at best, inconclusive. We integrate weekly incidence reports and a mechanistic transmission model within a likelihood-based inference framework to characterize the nature, timing, and magnitude of this interaction. We find support for a strong but short-lived interaction, with influenza infection increasing susceptibility to pneumococcal pneumonia ~100-fold. We infer modest population-level impacts arising from strong processes at the level of an individual, thereby resolving the dichotomy in seemingly inconsistent observations across scales. An accurate characterization of the influenza-pneumococcal interaction can form a basis for more effective clinical care and public health measures for pneumococcal pneumonia.
Biological approaches to mechanistically understand the healthy life span extension achieved by calorie restriction and modulation of hormones.

Calorie restriction and reduced somatotropic (growth hormone and insulin-like growth factor-1) signaling have a widespread though not universal ability to extend life. These interventions are considered central tools to understanding the downstream events that lead to the increase in healthy life span. As these approaches have been validated, the animals phenotyped, and the mechanisms proposed, many challenges have emerged. In this article, we give several examples and propose several considerations, opportunities, and approaches that may identify major mechanisms through which these interventions exert their effects, and which may lead to drug therapy to increase "health span. "
Exploring Maternal Emotion Masking as a Contribution to Kindergartener's Emotion Regulation

Parents socialize their child’s emotion regulation and expression through reactions and responses to, as well as discussion of, emotions during early childhood, around the same time children begin to express their thoughts and feelings verbally. The study of maternal emotion masking, or purposefully hiding an emotional expression, has produced mixed results regarding children’s emotion regulation. The current study examines maternal reports of children’s emotion regulation and mother’s use of monitoring and masking of emotions in relation to children’s expressive vocabulary during a story-telling task. Twenty-six mother-child dyads were recruited to engage in a story-telling task to examine children’s use of internal state language; mothers also completed questionnaires including the Emotion Regulation Checklist, Emotion Regulation Questionnaire, and the Parent Interview on Caregiving Infants. Children’s expressive vocabulary was additionally assessed using the Expressive Vocabulary Test, 2 Edition. Results suggest that mothers’ emotion monitoring relates to children’s greater use of emotion regulation and use of more positive words during story-telling. Mothers also differed in their use of emotion masking and monitoring by annual income and education level, which could be related to differences in highversus low-income stressors including more rigorous job demands. Future interventions should explore the effects of maternal emotion masking for parents who experience high stress levels.
Beyond Integrativeness: A Validation of the L2 Self Model among Francophone Learners of ESL

Abstract:According to Dörnyei’s model of second language (L2) motivation, the motivated learner aims to incorporate the L2 into his or her self-concept, known as the ideal L2 self. This study examined the internal consistency of Dörnyei’s model among ESL Francophone students in Quebec (n= 68) by means of a questionnaire. Correlations were calculated between factors measuring Gardner’s motivation construct, integrativeness, and Dörnyei’s ideal L2 self; both of these factors were then correlated with the criterion measure of intended learning effort. Findings from the present study revealed not only a strong relationship between Gardner’s integrativeness and Dörnyei’s ideal L2 self, but also that the L2 self construct was a more reliable indicator of intended learning effort. These results support calls to reframe L2 motivation within the psychological concept of the self. Résumé:Selon le modèle de Dörnyei sur la motivation en langue seconde (L2), l’apprenant motivé désire incorporer la L2 à son concept du « soi », connu comme le soi L2 idéal. La présente étude avait pour objectif de vérifier la fidélité interne du modèle de Dörnyei auprès d’une cohorte d’étudiants francophones en anglais L2 au Québec (n= 68) au moyen d’un questionnaire. Des corrélations ont été calculées entre les facteurs mesurant la dimension intégrative du modèle de Gardner et le soi L2 idéal de Dörnyei. Par la suite, l’indicateur le plus fiable de l’intention d’effort de l’apprenant, parmi ces deux construits, a été identifié. Les résultats de cette recherche ont révélé une corrélation entre le soi L2 idéal et la dimension intégrative. Ainsi, nos résultats appuient dans son intégrité le modèle de Dörnyei dans le contexte québécois. En effet, son construit central, le soi L2 idéal, s’est avéréêtre un indicateur fiable de l’intention de l’apprenant de déployer des efforts pour apprendre la L2. Ces résultats sont discutés au regard de la pertinence de resituer la motivation dans un cadre psychologique du soi.