Miracle-dz/UniFAR-FTUs huggingface dataset:
Renal dysfunction is a confounder for plasma natriuretic peptides in detecting heart dysfunction in uremic and idiopathic dilated cardiomyopathies.

BACKGROUND The diagnostic value of natriuretic peptides in uremic cardiomyopathy has not been defined, nor has the effect of a hemodialysis (HD) session on peptides. METHODS We performed an observational study of 100 white adult outpatients in New York Heart Association class I-II, with neither diabetes nor ischemic heart disease, 50 of whom had idiopathic dilated cardiomyopathy (DCM) and 50 of whom had uremic cardiomyopathy and were undergoing HD. We measured plasma N-terminal proB-type natriuretic peptide (NT-proBNP), BNP, and atrial natriuretic peptide (ANP) both before and after a dialysis session. Doppler echocardiograms were evaluated. We performed multiple regression analysis on the logarithm of peptide concentrations using clinical, laboratory, and echocardio-Doppler data as explanatory variables. RESULTS Mean peptide concentrations were higher in the HD group, with an HD:DCM ratio of 25 for NT-proBNP and 5 for BNP and ANP. Peptides were correlated with each other (r > 0.85). After HD, NT-proBNP significantly increased by 14%, BNP decreased by 17%, and ANP decreased by 56%. Predialysis concentrations correlated with postdialysis values (r > 0.85). A multiple regression equation significantly fitted the observed peptide concentrations, both pre- and postdialysis, using the same set of 4 variables: disease group (DCM or HD), diastolic pattern, left atrial volume, and body mass index. CONCLUSIONS Renal dysfunction was a confounder for natriuretic peptides, which were present in higher concentrations in the uremic patients with milder cardiac dysfunction than in those with idiopathic DCM without renal dysfunction. Left diastolic function pattern and atrial volume were cardiac determinants of peptide concentrations in DCM and HD.
Correlation of MRI findings and cognitive function in multiple sclerosis patients using montreal cognitive assessment test

Background: Magnetic resonance imaging (MRI) has improved the diagnosis and management of patients with multiple sclerosis (MS). Montreal Cognitive Assessment (MoCA) is a brief, sensitive test that has been recommended by National Institute of Neurological Diseases and Stroke and Canadian Stroke Network (NINDS-CSN) as a reliable tool to detect mild cognitive impairments. This study aimed to evaluate the relationship between MoCA test and its sub-items with brain abnormalities in MRI of MS patients. Methods: Based on MRI scans of 46 MS patients, third ventricle and white matter lesions volumes were measured. Disease duration and expanded disability status scale (EDSS) were recorded in each patient. In addition, cognitive domains of the patients were evaluated by Montreal cognitive assessment (MoCA) test. We analyzed data using t-test or Mann-Whitney U test, Pearson correlation coefficient, and non-parametric Spearman test. Furthermore, multiple linear regression model was applied to evaluate the association between cognitive indices and MRI characteristics. Results: Among MRI indices, only severity of atrophy showed a significant difference between cognitively impaired and cognitively preserved patients. Third ventricular volume was significantly correlated with total MoCA score (p=0.003, r=-0.42), but none of the juxtacortical or periventricular lesions volume revealed significant relation with total MoCA score. However, using multivariate linear regression after adjustment for educational level and disease duration, there was a significant negative association between juxtacortical lesions volume and total MoCA score as well as naming and attention sub-items. Also, memory score was adversely associated with the third ventricular volume (p=0.03, r=0.31). Conclusion: Cognitive disturbances detected by MoCA, may be associated with some pathological changes including atrophy, third ventricular volume, and juxtacortical lesion. MoCA, as a brief test, is not correlated with brain lesions volume in MS patients.
Improving Incentives for Clean Vehicle Purchases in the United States: Challenges and Opportunities

In recent decades, federal and state policymakers in the United States have adopted a variety of policy incentives to induce drivers to purchase advanced clean vehicles aimed at reducing externalities within the transportation sector. Focusing on plug-in electric vehicles, I examine the challenges to and opportunities for improving these policies. Recent research raises concerns about whether the incentives actually reach the intended consumers because of eligibility restrictions, salience of instruments in consumer decision making, and the impact of incentives across consumers and producers. The targeting of different externalities complicates policy design choices, which are further limited because purchase incentives do not affect driving behavior. Finally, an emerging literature suggests that the efficiency and cost effectiveness of these incentives may be improved by strategically targeting specific types of vehicles and consumers, as well as by combining them with vehicle retirement incentives. (JEL: Q53, Q55, R40)
TANK-Binding Kinase 1 Attenuates PTAP-Dependent Retroviral Budding through Targeting Endosomal Sorting Complex Required for Transport-I

Retroviruses need to bud from producer cells to spread infection. To facilitate its budding, some virus hijacks the multivesicular body (MVB) pathway that is normally used to cargo and degrade ubiquitylated cellular proteins, through interaction between the late domain of Gag polyproteins and the components of MVB machinery. In this study, we demonstrated that TANK-binding kinase 1 (TBK1) directly interacted with VPS37C, a subunit of endosomal sorting complex required for transport-I (ESCRT-I) in the MVB pathway, without affecting the ultrastructure or general function of MVB. Interestingly, overexpression of TBK1 attenuated, whereas short hairpin RNA interference of TBK1 enhanced HIV-1 pseudovirus release from Vero cells in type I IFN (IFN-I)-independent manner. Down-regulation of TBK1 by short hairpin RNA in TZM-bl cells also enhanced live HIV-1 NL4-3 or JR-CSF virus budding without involvement of IFN-I induction. Furthermore, infection of TBK1-deficient mouse embryonic fibroblast cells with a chimeric murine leukemia virus/p6, whose PPPY motif was replaced by PTAP motif of HIV-1, showed that lack of TBK1 significantly enhanced PTAP-dependent, but not PPPY-dependent retrovirus budding. Finally, phosphorylation of VPS37C by TBK1 might regulate the viral budding efficiency, because overexpression of the kinase-inactive mutant of TBK1 (TBK1-K38A) in Vero cells accelerated HIV-1 pseudovirus budding. Therefore, through tethering to VPS37C of the ESCRT-I complex, TBK1 controlled the speed of PTAP-dependent retroviral budding through phosphorylation of VPS37C, which would serve as a novel mechanism of host cell defense independent of IFN-I signaling.
5G new RAT uplink control channel for small payloads

In this paper, channel design for the New Radio (NR) physical uplink control channel (NR PUCCH) of 1 symbol (short-PUCCH) carrying up to 2 bits of acknowledgement (ACK)/negative ACK (NACK) is investigated. Two types of short-PUCCH designs, i.e., short-PUCCH type A and short-PUCCH type B, are compared and evaluated by computer simulation. In short-PUCCH type A, reference signal (RS) and ACK/NACK are multiplexed in different subcarriers within the same symbol; in short-PUCCH type B, no RS is used and ACK/NACK are indicated by which sequence is selected among the sequence candidates. The link-level evaluation results and link-budget analysis show that short-PUCCH type B has 40∼60 % larger coverage than short-PUCCH type A.
Simulation on dynamic arc-before process of large current vacuum breaking

Arc breaking at the function of large current is one of the bottlenecks for the development of vacuum breaker to higher voltage level and it is also the hotspot nowadays. Seen from the reasons of arc igniting and its influencing factors, arc-before process from the contacts separating to stable arc igniting is the base of arc research. Arc-before process model of vacuum circuit breaker is developed here based on gas dynamic equation. Its breaking current is 20kA and clearance is 10mm. Collisions between charged particles and metal vapor and electrodes are considered in the simulation. The physical nature of the sheath and arc column's formation, the space charge densities and their effects on electric field strength before the steady state of arc plasma are simulated here. The simulations in this paper lay the foundations for depth understanding of vacuum arc plasma's formation mechanism and it also improves people's knowledge of arc igniting process which will benefit for exploring effective method to control and quench arc.
A Causative Relationship Exists Between Eosinophils and the Development of Allergic Pulmonary Pathologies in the Mouse1

Asthma and mouse models of allergic respiratory inflammation are invariably associated with a pulmonary eosinophilia; however, this association has remained correlative. In this report, a causative relationship between eosinophils and allergen-provoked pathologies was established using eosinophil adoptive transfer. Eosinophils were transferred directly into the lungs of either naive or OVA-treated IL-5−/− mice. This strategy resulted in a pulmonary eosinophilia equivalent to that observed in OVA-treated wild-type animals. A concomitant consequence of this eosinophil transfer was an increase in Th2 bronchoalveolar lavage cytokine levels and the restoration of intracellular epithelial mucus in OVA-treated IL-5−/− mice equivalent to OVA-treated wild-type levels. Moreover, the transfer also resulted in the development of airway hyperresponsiveness. These pulmonary changes did not occur when eosinophils were transferred into naive IL-5−/− mice, eliminating nonspecific consequences of the eosinophil transfer as a possible explanation. Significantly, administration of OVA-treated IL-5−/− mice with GK1.5 (anti-CD4) Abs abolished the increases in mucus accumulation and airway hyperresponsiveness following adoptive transfer of eosinophils. Thus, CD4+ T cell-mediated inflammatory signals as well as signals derived from eosinophils are each necessary, yet alone insufficient, for the development of allergic pulmonary pathology. These data support an expanded view of T cell and eosinophil activities and suggest that eosinophil effector functions impinge directly on lung function.
Follicular Dendritic Cells Activate HIV-1 Replication in Monocytes/Macrophages through a Juxtacrine Mechanism Mediated by P-Selectin Glycoprotein Ligand 11

Follicular dendritic cells (FDCs) are located in the lymphoid follicles of secondary lymphoid tissues and play a pivotal role in the selection of memory B lymphocytes within the germinal center, a major site for HIV-1 infection. Germinal centers are composed of highly activated B cells, macrophages, CD4+T cells, and FDCs. However, the physiological role of FDCs in HIV-1 replication remains largely unknown. We demonstrate in our current study that FDCs can efficiently activate HIV-1 replication in latently infected monocytic cells via an intercellular communication network mediated by the P-selectin/P-selectin glycoprotein ligand 1 (PSGL-1) interaction. Upon coculture with FDCs, HIV-1 replication was significantly induced in infected monocytic cell lines, primary monocytes, or macrophages. These cocultures were found to synergistically induce the expression of P-selectin in FDCs via NF-κB activation and its cognate receptor PSGL-1 in HIV-1-infected cells. Consistent with this observation, we find that this response is significantly blocked by antagonistic Abs against PSGL-1 and almost completely inhibited by PSGL-1 small interfering RNA. Moreover, a selective inhibitor for Syk, which is a downstream effector of PSGL-1, blocked HIV-1 replication in our cultures. We have thus elucidated a novel regulatory mechanism in which FDCs are a potent positive bystander that facilitates HIV-1 replication in adjacent infected monocytic cells via a juxtacrine signaling mechanism.
Effect of neighborhood environment and individual social integration on mortality risk: an analysis of the Third National Health and Nutrition Examination Survey (NHANES III)

Background: There is a growing body of literature linking neighborhood contexts to health. Studies examining neighborhood socioeconomic status (SES) and mortality have shown a consistent, though not always significant, association between low neighborhood SES and increased mortality risk. The present study aimed to assess the relationship between neighborhood poverty and mortality risk among adults in the Third National Health and Nutrition Examination Survey (NHANES III), a national probability sample. METHODS: We examined data from the NHANES III geocoded and matched to census tracts, serving as neighborhood proxies. We operationalized neighborhood poverty as the proportion of residents in a census tract living below the federal poverty level. We analyzed data using Kaplan-Meier survival curves as well as Cox proportional hazards regression models that accounted for the complex survey design. RESULTS: Living in a low poverty neighborhood was consistently associated with a lower mortality risk when compared to living in a high poverty (≥20%) neighborhood in this sample. Men living in high poverty neighborhoods had 1.29 (95% confidence interval: 1.01, 1.64) times the risk of death of men living in low (<5%) poverty neighborhoods. DISCUSSION: A positive association between neighborhood poverty and mortality risk was seen in this national probability sample, particularly among men. This finding
Non-Affine GARCH Option Pricing Models, Variance Dependent Kernels, and Diffusion Limits

This paper investigates the pricing and weak convergence of an asymmetric non-affine, non-Gaussian GARCH model when the risk-neutralization is based on a variance dependent exponential linear pricing kernel with stochastic risk aversion parameters. The risk-neutral dynamics are obtained for a general setting and its weak limit is derived. We show how several GARCH diffusions, martingalized via well-known pricing kernels, are obtained as special cases and we derive necessary and sufficient conditions for the presence of financial bubbles. An extensive empirical analysis using both historical returns and options data illustrates the advantage of coupling this pricing kernel with non-Gaussian innovations.
Gestion collective des inondations. Peut-on tenir compte de l'avis de la population dans la phase d'évaluation économique a priori ?

En France, au contraire de pays comme les Etats-Unis, la pratique de l'evaluation economique a priori des actions collectives de lutte contre les inondations est largement deficiente. Ce constat est inquietant dans une perspective d'allocation optimale de ressources necessairement limitees. Quand elle existe, cette evaluation n'integre pas les preferences des populations affectees. Ce manque est a contre-courant des preconisations de la convention d'Aarhus signee par la France. Dans cette these, l'apport envisageable de l'evaluation contingente est exploree. Deux enquetes ont ete realisees, sur deux terrains aux caracteristiques contrastees : sur le bassin versant de l'Yzeron (zone peri-urbaine sur un petit bassin versant aux crues rapides et aux enjeux humains forts) et au Mans (zone urbaine a la confluence de la Sarthe et de l'Huisne aux crues lentes et aux enjeux humains faibles). Inscrite dans une perspective d'evaluation a priori de differents niveaux de protection collective, la realisation de ces enquetes a necessite l'elaboration d'un outil de communication permettant une description, accessible aux non-experts, des effets des scenarios contingents sur le degre d'exposition d'une collectivite aux inondations. L'analyse des enquetes permet un certain nombre d'analyses critiques quant aux choix methodologiques employes (impact du choix des taxes locales comme support de paiement sur le taux de refus par exemple). Elle permet egalement de degager un comportement des individus interprete comme une acceptabilite du risque d'inondation au-dela d'un certain niveau de protection. Confirmee, cette conclusion aurait un impact direct sur la necessite de pratiquer enfin une evaluation economique a priori des actions collectives de lutte contre les inondations, integrant de surcroit explicitement les preferences des populations affectees.
Longitudinal predictors of progression of carotid atherosclerosis in rheumatoid arthritis.

OBJECTIVE To explore predictors of change in measures of carotid atherosclerosis among rheumatoid arthritis (RA) patients without known cardiovascular disease (CVD) at baseline. METHODS RA patients underwent carotid ultrasonography at 2 time points separated by a mean ± SD of 3.2 ± 0.3 years. The associations of baseline and average patient characteristics with the average yearly change in the mean maximal intima-media thickness (IMT) of the common carotid artery (CCA) and the internal carotid artery (ICAs) and with incident or progressive plaque in the ICA/carotid bulb, were explored. RESULTS Among the 158 RA patients, the maximal CCA-IMT increased in 82% (median 16 μm/year; P < 0.001) and the maximal ICA-IMT increased in 70% (median 25 μm/year; P < 0.001). Incident plaque was observed in 14% of those without plaque at baseline (incidence rate 4.2 per 100 person-years [95% confidence interval 1.6, 6.8]). Plaque progression was observed in 5% of those with plaque at baseline. Among RA predictors, the adjusted average yearly change in the maximal CCA-IMT was significantly greater in patients with earlier RA than in those with disease of longer duration. Those taking tumor necrosis factor (TNF) inhibitors at baseline had a 37% lower adjusted rate of progression in the maximal CCA-IMT compared with nonusers (14 μm/year versus 22 μm/year; P = 0.026). For the maximal ICA-IMT, cumulative prednisone exposure was associated with progression after adjustment (1.2 μm/year per gm [95% confidence interval 0.1, 2.4]) and was lower in patients who were prescribed statins concomitant with prednisone. Higher swollen joint counts and higher average C-reactive protein levels were both associated with incident or progressive plaque, primarily in patients with elevated CVD risk at baseline based on the Framingham Risk Score. CONCLUSION These prospective data provide evidence that inflammation is a contributor to the progression of subclinical atherosclerosis in RA and that it is potentially modified favorably by TNF inhibitors and detrimentally by glucocorticoids.
A Moloney Murine Leukemia Virus-Based Retrovirus with 4070A Long Terminal Repeat Sequences Induces a High Incidence of Myeloid as Well as Lymphoid Neoplasms

ABSTRACT Retroviruses can be used to accelerate hematopoietic cancers predisposed to neoplastic disease by prior genetic manipulations such as in transgenic or knockout mice. The virus imparts a second neoplastic “hit,” providing evidence that the initial hit is transforming. In the present study, a unique retrovirus was developed that can induce a high incidence of myeloid disease and has a broad host range. This agent is a Moloney murine leukemia virus (Mo-MuLV)-based virus that has most of the U3 region of the long terminal repeat (LTR) replaced with that of retrovirus 4070A. Like Mo-MuLV, this virus, called MOL4070LTR, is NB-tropic and not restricted by Fv1 allelles. MOL4070LTR causes myeloid leukemias in ca. 50% of mice, a finding in contrast to Mo-MuLV, which induces almost exclusively lymphoid disease. The data suggest that the LTR of the 4070A virus expands the tissue tropism of the disease to the myeloid lineage. Interesting, MCF recombinant envelope was expressed in the lymphoid but not the myeloid neoplasms of BALB/c mice. This retrovirus has the potential for accelerating myeloid disease in genetically engineered mice.
Proteomic Identification and Functional Characterization of a Novel ARF6 GTPase-activating Protein, ACAP4*S

ARF6 GTPase is a conserved regulator of membrane trafficking and actin-based cytoskeleton dynamics at the leading edge of migrating cells. A key determinant of ARF6 function is the lifetime of the GTP-bound active state, which is orchestrated by GTPase-activating protein (GAP) and GTP-GDP exchanging factor. However, very little is known about the molecular mechanisms underlying ARF6-mediated cell migration. To systematically analyze proteins that regulate ARF6 activity during cell migration, we performed a proteomic analysis of proteins selectively bound to active ARF6 using mass spectrometry and identified a novel ARF6-specific GAP, ACAP4. ACAP4 encodes 903 amino acids and contains two coiled coils, one pleckstrin homology domain, one GAP motif, and two ankyrin repeats. Our biochemical characterization demonstrated that ACAP4 has a phosphatidylinositol 4,5-bisphosphate-dependent GAP activity specific for ARF6. The co-localization of ACAP4 with ARF6 occurred in ruffling membranes formed upon AIF4 and epidermal growth factor stimulation. ACAP4 overexpression limited the recruitment of ARF6 to the membrane ruffles in the absence of epidermal growth factor stimulation. Expression of GTP hydrolysis-resistant ARF6Q67L resulted in accumulations of ACAP4 and ARF6 in the cytoplasmic membrane, suggesting that GTP hydrolysis is required for the ARF6-dependent membrane remodeling. Significantly the depletion of ACAP4 by small interfering RNA or inhibition of ARF6 GTP hydrolysis by overexpressing GAP-deficient ACAP4 suppressed ARF6-dependent cell migration in wound healing, demonstrating the importance of ACAP4 in cell migration. Thus, our study sheds new light on the biological function of ARF6-mediated cell migration.
COMPARISON OF NON‐GAUSSIAN QUANTITATIVE GENETIC MODELS FOR MIGRATION AND STABILIZING SELECTION

The balance between stabilizing selection and migration of maladapted individuals has formerly been modeled using a variety of quantitative genetic models of increasing complexity, including models based on a constant expressed genetic variance and models based on normality. The infinitesimal model can accommodate nonnormality and a nonconstant genetic variance as a result of linkage disequilibrium. It can be seen as a parsimonious one‐parameter model that approximates the underlying genetic details well when a large number of loci are involved. Here, the performance of this model is compared to several more realistic explicit multilocus models, with either two, several or a large number of alleles per locus with unequal effect sizes. Predictions for the deviation of the population mean from the optimum are highly similar across the different models, so that the non‐Gaussian infinitesimal model forms a good approximation. It does, however, generally estimate a higher genetic variance than the multilocus models, with the difference decreasing with an increasing number of loci. The difference between multilocus models depends more strongly on the effective number of loci, accounting for relative contributions of loci to the variance, than on the number of alleles per locus.