Miracle-dz/UniFAR-FTUs huggingface dataset:
A Self-Regulatory Circuit of CIRCADIAN CLOCK-ASSOCIATED1 Underlies the Circadian Clock Regulation of Temperature Responses in Arabidopsis[W]

The CCA1 MYB transcription factor is a component of the circadian clock, which plays an important role in plant responses to cold temperatures. This work shows that cold temperatures regulate CCA1 activity by modulating CCA1 alternative splicing and thus altering the molecular ratios of alternatively spliced isoforms to induce cold tolerance responses. The circadian clock synchronizes biological processes to daily cycles of light and temperature. Clock components, including CIRCADIAN CLOCK-ASSOCIATED1 (CCA1), are also associated with cold acclimation. However, it is unknown how CCA1 activity is modulated in coordinating circadian rhythms and cold acclimation. Here, we report that self-regulation of Arabidopsis thaliana CCA1 activity by a splice variant, CCA1β, links the clock to cold acclimation. CCA1β interferes with the formation of CCA1α-CCA1α and LATE ELONGATED HYPOCOTYL (LHY)-LHY homodimers, as well as CCA1α-LHY heterodimers, by forming nonfunctional heterodimers with reduced DNA binding affinity. Accordingly, the periods of circadian rhythms were shortened in CCA1β-overexpressing transgenic plants (35S:CCA1β), as observed in the cca1 lhy double mutant. In addition, the elongated hypocotyl and leaf petiole phenotypes of CCA1α-overexpressing transgenic plants (35S:CCA1α) were repressed by CCA1β coexpression. Notably, low temperatures suppressed CCA1 alternative splicing and thus reduced CCA1β production. Consequently, whereas the 35S:CCA1α transgenic plants exhibited enhanced freezing tolerance, the 35S:CCA1β transgenic plants were sensitive to freezing, indicating that cold regulation of CCA1 alternative splicing contributes to freezing tolerance. On the basis of these findings, we propose that dynamic self-regulation of CCA1 underlies the clock regulation of temperature responses in Arabidopsis.
Self-Healing Key Distribution with Revocation and Collusion Resistance for Wireless Sensor Networks

Self-healing key distribution enables users in a large and dynamic group to establish session keys for secure group communication over an unreliable network (e.g., wireless sensor networks). The main property of self-healing key distribution is that the users are capable of recovering lost session keys on their own, without requesting additional transmissions from the group manager. In this paper, we propose a self-healing key distribution scheme with t-revocation and 2t-collusion resistance capabilities for wireless sensor networks. Built on an appropriate security model, our scheme reduces both storage and communication overhead and eliminates the limitations of m sessions when compared with some previous work under the same security model. In addition, we propose a scheme which enables key recovery from a single broadcast message.
Drug-eluting stents for acute myocardial infarction

This is a review of the literature comparing the efficacy and safety of drug-eluting stents (DES) versus bare-metal stents (BMS) in patients with acute myocardial infarction (MI). The present article reviews whether DES are beneficial in the setting of primary percutaneous coronary intervention (PCI), and this has been the subject of many recent publications and debate among clinicians. To the best of our knowledge there are limited registries and randomized trials about DES for acute MI in the English literature. Bare-metal stents have a higher incidence of instent restenosis whereas DES might have a slightly higher late thrombosis risk. With the current data DES might still have an advantage over BMS in the treatment of ST-segment elevation MI (STEMI) patients with the vastly improved target vessel revascularization rates. Despite the lack of well-designed head-to-head long-term prospective clinical trials, DES may not be effective in patients who are on short-term dual antiplatelet therapy owing to an increased risk of late stent thrombosis. In conclusion, DES use in STEMI patients continuing long-term dual antiplatelet therapy is safe and effective.
A capsule conjugate vaccine approach to prevent diarrheal disease caused by Campylobacter jejuni

Campylobacter jejuni is a major cause of diarrheal disease and results in high levels of morbidity and economic loss in both industrialized and developing regions of the world. To date, prior vaccine approaches have failed to confer protection against this enteric pathogen. Key challenges to the development of a practical Campylobacter vaccine for human use include a lack of understanding of Campylobacter pathogenesis and well-defined immune correlates of protection. With the discovery that C. jejuni expresses a capsule polysaccharide associated with virulence, a conjugate vaccine approach is currently being evaluated. Conjugate vaccines have been successfully developed and implemented against other invasive mucosal pathogens including Streptococcus pneumoniae, Neisseria meningitidis,and Hemophilus influenzae. Furthermore, Shigella-based conjugate vaccines based on lipopolysaccharide have shown promising results in field trials. A prototype C. jejuni conjugate vaccine is currently entering human testing.
Classification of a frameshift/extended and a stop mutation in WT1 as gain-of-function mutations that activate cell cycle genes and promote Wilms tumour cell proliferation

The WT1 gene encodes a zinc finger transcription factor important for normal kidney development. WT1 is a suppressor for Wilms tumour development and an oncogene for diverse malignant tumours. We recently established cell lines from primary Wilms tumours with different WT1 mutations. To investigate the function of mutant WT1 proteins, we performed WT1 knockdown experiments in cell lines with a frameshift/extension (p.V432fsX87 = Wilms3) and a stop mutation (p.P362X = Wilms2) of WT1, followed by genome-wide gene expression analysis. We also expressed wild-type and mutant WT1 proteins in human mesenchymal stem cells and established gene expression profiles. A detailed analysis of gene expression data enabled us to classify the WT1 mutations as gain-of-function mutations. The mutant WT1Wilms2 and WT1Wilms3 proteins acquired an ability to modulate the expression of a highly significant number of genes from the G2/M phase of the cell cycle, and WT1 knockdown experiments showed that they are required for Wilms tumour cell proliferation. p53 negatively regulates the activity of a large number of these genes that are also part of a core proliferation cluster in diverse human cancers. Our data strongly suggest that mutant WT1 proteins facilitate expression of these cell cycle genes by antagonizing transcriptional repression mediated by p53. We show that mutant WT1 can physically interact with p53. Together the findings show for the first time that mutant WT1 proteins have a gain-of-function and act as oncogenes for Wilms tumour development by regulating Wilms tumour cell proliferation.
Rational Bias in Macroeconomic Forecasts

This paper develops a model of macroeconomic forecasting in which the wages firms pay their forecasters are a function of their accuracy as well as the publicity they generate for their employers by being correct. In the resulting Nash equilibrium, forecasters with identical models, information, and incentives nevertheless produce a variety of predictions in order to maximize their expected wages. In the case of heterogeneous incentives, the forecasters whose wages are most closely tied to publicity, as opposed to accuracy, produce the forecasts that deviate most from the consensus. We find empirical support for our model using a twenty-year panel of real GNP/GDP forecast data from the survey Blue Chip Economic Indicators. Although the consensus outperforms virtually every forecaster, many forecasters choose to deviate from it substantially and regularly. Moreover, the extent of this deviation varies by industry in a manner consistent with our model.
Galaxy And Mass Assembly (GAMA) : the bright void galaxy population in the optical and mid-IR.

We examine the properties of galaxies in the Galaxies and Mass Assembly (GAMA) survey located in voids with radii >10 h−1 Mpc. Utilizing the GAMA equatorial survey, 592 void galaxies are identified out to z ≈ 0.1 brighter than Mr = −18.4, our magnitude completeness limit. Using the WHα versus [N ii]/Hα (WHAN) line strength diagnostic diagram, we classify their spectra as star forming, AGN, or dominated by old stellar populations. For objects more massive than 5 × 109 M⊙, we identify a sample of 26 void galaxies with old stellar populations classed as passive and retired galaxies in the WHAN diagnostic diagram, else they lack any emission lines in their spectra. When matched to Wide-field Infrared Survey Explorer mid-IR photometry, these passive and retired galaxies exhibit a range of mid-IR colour, with a number of void galaxies exhibiting [4.6] − [12] colours inconsistent with completely quenched stellar populations, with a similar spread in colour seen for a randomly drawn non-void comparison sample. We hypothesize that a number of these galaxies host obscured star formation, else they are star forming outside of their central regions targeted for single-fibre spectroscopy. When matched to a randomly drawn sample of non-void galaxies, the void and non-void galaxies exhibit similar properties in terms of optical and mid-IR colour, morphology, and star formation activity, suggesting comparable mass assembly and quenching histories. A trend in mid-IR [4.6] − [12] colour is seen, such that both void and non-void galaxies with quenched/passive colours <1.5 typically have masses higher than 1010 M⊙, where internally driven processes play an increasingly important role in galaxy evolution.
Matrix stiffness reverses the effect of actomyosin tension on cell proliferation

Summary The stiffness of the extracellular matrix exerts powerful effects on cell proliferation and differentiation, but the mechanisms transducing matrix stiffness into cellular fate decisions remain poorly understood. Two widely reported responses to matrix stiffening are increases in actomyosin contractility and cell proliferation. To delineate their relationship, we modulated cytoskeletal tension in cells grown across a physiological range of matrix stiffnesses. On both synthetic and naturally derived soft matrices, and across a panel of cell types, we observed a striking reversal of the effect of inhibiting actomyosin contractility, switching from the attenuation of proliferation on rigid substrates to the robust promotion of proliferation on soft matrices. Inhibiting contractility on soft matrices decoupled proliferation from cytoskeletal tension and focal adhesion organization, but not from cell spread area. Our results demonstrate that matrix stiffness and actomyosin contractility converge on cell spreading in an unexpected fashion to control a key aspect of cell fate.
Structure of the human type XIX collagen (COL19A1) gene, which suggests it has arisen from an ancestor gene of the FACIT family.

Type XIX collagen is a newly discovered member of the FACIT (fibril-associated collagens with interrupted triple helices) group of extracellular matrix proteins. Based on the primary structure, type XIX collagen is thought to act as a cross-bridge between fibrils and other extracellular matrix molecules. Here we describe the complete exon/intron organization of COL19A1 and show that it contains 51 exons, spanning more than 250 kb of genomic DNA. The comparison of exon structures of COL19A1 and other FACIT family genes revealed several similarities among these genes. The structure of exons encoding the noncollagenous (NC) 1-collagenous (COL) 1-NC 2-COL 2-NC 3-COL 3-NC 4 domain of the alpha1(XIX) chain is similar to that of the NC 1-COL 1-NC 2-COL 3-NC 3 domain of the alpha2(IX) chain except for the NC 3 domain of alpha1(XIX). The exons encoding the COL 5-NC 6 domain of alpha1(XIX) are also similar to those of the COL 3-NC 4 domain of alpha1(IX) chain. Previously, COL19A1 was mapped to human chromosome 6q12-q14, where COL9A1 is also located. Likewise, the present work shows that the mouse Col19a1 gene is located on mouse chromosome 1, region A3, where Col9a1 has also been mapped. Taken together, the data suggest that COL19A1 and COL9A1 (Col19a1 and Col9a1) were duplicated from the same ancestor gene of the FACIT family. Three CA repeat markers with high heterozygosity were found in COL19A1. These markers may be useful for linkage analysis of age-related inheritable diseases involved in eyes and/or brain.
Simultaneous Live Cell Imaging Using Dual FRET Sensors with a Single Excitation Light

Fluorescence resonance energy transfer (FRET) between fluorescent proteins is a powerful tool for visualization of signal transduction in living cells, and recently, some strategies for imaging of dual FRET pairs in a single cell have been reported. However, these necessitate alteration of excitation light between two different wavelengths to avoid the spectral overlap, resulting in sequential detection with a lag time. Thus, to follow fast signal dynamics or signal changes in highly motile cells, a single-excitation dual-FRET method should be required. Here we reported this by using four-color imaging with a single excitation light and subsequent linear unmixing to distinguish fluorescent proteins. We constructed new FRET sensors with Sapphire/RFP to combine with CFP/YFP, and accomplished simultaneous imaging of cAMP and cGMP in single cells. We confirmed that signal amplitude of our dual FRET measurement is comparable to of conventional single FRET measurement. Finally, we demonstrated to monitor both intracellular Ca2+ and cAMP in highly motile cardiac myocytes. To cancel out artifacts caused by the movement of the cell, this method expands the applicability of the combined use of dual FRET sensors for cell samples with high motility.
Fully analog self-mixing laser vibrometer

This work concerns the implementation of a fully analog vibrometer utilizing self-mixing interferometric technique. Its working principle is a sort of unwrap of the interferometric signal: by analog elaborations the jumps of the signal are compensated. The sensor exploits the linearity of a single interferometric fringe, achieving resolution much better than half a wavelength, over a wide displacement range. The realized sensor combines a very simple optical setup with a low cost electronic elaboration, allowing excellent performances: 1 mm of range measurement with 35 nm resolution, 10 kHz bandwidth, obtained with very low material cost, including the optical and electronics components.
Appendix for : Do Oil Windfalls Improve Living Standards ? Evidence from Brazil

The total amount of royalty payments from each oilfield is the sum of two components. The first component is a fixed 5% of the value of the oil extracted. We call it the fixed quota. The second is a further percentage that must be between 0 and 5%. We call this the variable quota. However, even the variable quota is almost always set at the maximum of 5%. This is because the legislation authorizes ANP to assign a quota less than the maximum only in the case of lowerquality or higher-risk fields. As a result about 90% of the oilfields and all of the large oilfields pay between 9.1 and 10% in royalties. Another 9% pays between 8.1 and 9%. Only 1% pays less than 8%. The weighted average royalty is 9.8%.
Effects of Three Types of Resisted Sprint Training Devices on the Kinematics of Sprinting at Maximum Velocity

Resisted sprint running is a common training method for improving sprint-specific strength. For maximum specificity of training, the athlete's movement patterns during the training exercise should closely resemble those used when performing the sport. The purpose of this study was to compare the kinematics of sprinting at maximum velocity to the kinematics of sprinting when using three of types of resisted sprint training devices (sled, parachute, and weight belt). Eleven men and 7 women participated in the study. Flying sprints greater than 30 m were recorded by video and digitized with the use of biomechanical analysis software. The test conditions were compared using a 2-way analysis of variance with a post-hoc Tukey test of honestly significant differences. We found that the 3 types of resisted sprint training devices are appropriate devices for training the maximum velocity phase in sprinting. These devices exerted a substantial overload on the athlete, as indicated by reductions in stride length and running velocity, but induced only minor changes in the athlete's running technique. When training with resisted sprint training devices, the coach should use a high resistance so that the athlete experiences a large training stimulus, but not so high that the device induces substantial changes in sprinting technique. We recommend using a video overlay system to visually compare the movement patterns of the athlete in unloaded sprinting to sprinting with the training device. In particular, the coach should look for changes in the athlete's forward lean and changes in the angles of the support leg during the ground contact phase of the stride.
Experimental investigation of the shearing resistance of SODA-Lime glass at pressures of 9 GPa and strain rates of 10^6 s^(-1)

Pressure-Shear Plate Impact (PSPI) experiments were conducted to measure the high-rate shearing resistance of soda-lime glass at pressures of 9 GPa and at shearing rates of approximately 10^6 s^(−1). Samples of soda lime glass, 5 µm thick, were sandwiched between pure tungsten carbide (WC) plates and impacted by pure WC flyers. Impacting plates were inclined to the direction of approach by an angle of 18°. Normal stress and shearing resistance of the sample were calculated from measured free surface velocities using 1D elastic wave theory. The experimental results show that, at a pressure of 9GPa, the shear stress increases almost linearly up to 1 GPa and then falls quickly to approximately 0.3 GPa — after which it decreases slowly to approximately 0.17 GPa. Comparisons with results of previous experiments on nominally identical samples, impacted to generate lower peak pressures, showed the peak shearing resistance to be much higher at higher pressures; however, the sharp fall in shearing resistance occurs at comparable shear strains (1.5-2).
Biochemical Studies on Methylglyoxal-Mediated Glycated Histones: Implications for Presence of Serum Antibodies against the Glycated Histones in Patients with Type 1 Diabetes Mellitus

Reactive carbonyl species (RCS) mainly reacts with lysine and arginine residues of proteins to form advanced glycation end products (AGEs). Histone was glycoxidated with glyoxal and methylglyoxal. It was characterized by polyacrylamide gel electrophoresis and quenching studies involving penicillamine and aminoguanidine as carbonyl scavengers. Further characterization of histone modified with methylglyoxal was done by UV, fluorescence, and IR spectrophotometry. Spectral analysis of the protein clearly demonstrates structural perturbation in the histone by methylglyoxal. Methylglyoxal-induces cross-linking in the protein leading to aggregation. Role of methylglyoxal mediated glycoxidation of histone in type 1 diabetes was also undertaken. Antibodies were detected against glycoxidated histone in sera of type 1 diabetes patients by solid-phase enzyme immunoassay. The findings indicate that as a result of structural perturbation in histone by methylglyoxal, the modified histone may be involved in production of serum antibodies in the diabetes patients.
Policy Interventions to Promote Healthy Eating: A Review of What Works, What Does Not, and What is Promising

Unhealthy diets can lead to various diseases, which in turn can translate into a bigger burden for the state in the form of health services and lost production. Obesity alone has enormous costs and claims thousands of lives every year. Although diet quality in the European Union has improved across countries, it still falls well short of conformity with the World Health Organization dietary guidelines. In this review, we classify types of policy interventions addressing healthy eating and identify through a literature review what specific policy interventions are better suited to improve diets. Policy interventions are classified into two broad categories: information measures and measures targeting the market environment. Using this classification, we summarize a number of previous systematic reviews, academic papers, and institutional reports and draw some conclusions about their effectiveness. Of the information measures, policy interventions aimed at reducing or banning unhealthy food advertisements generally have had a weak positive effect on improving diets, while public information campaigns have been successful in raising awareness of unhealthy eating but have failed to translate the message into action. Nutritional labeling allows for informed choice. However, informed choice is not necessarily healthier; knowing or being able to read and interpret nutritional labeling on food purchased does not necessarily result in consumption of healthier foods. Interventions targeting the market environment, such as fiscal measures and nutrient, food, and diet standards, are rarer and generally more effective, though more intrusive. Overall, we conclude that measures to support informed choice have a mixed and limited record of success. On the other hand, measures to target the market environment are more intrusive but may be more effective.
PINK1-Parkin Pathway Activity Is Regulated by Degradation of PINK1 in the Mitochondrial Matrix

Loss-of-function mutations in PINK1, which encodes a mitochondrially targeted serine/threonine kinase, result in an early-onset heritable form of Parkinson's disease. Previous work has shown that PINK1 is constitutively degraded in healthy cells, but selectively accumulates on the surface of depolarized mitochondria, thereby initiating their autophagic degradation. Although PINK1 is known to be a cleavage target of several mitochondrial proteases, whether these proteases account for the constitutive degradation of PINK1 in healthy mitochondria remains unclear. To explore the mechanism by which PINK1 is degraded, we performed a screen for mitochondrial proteases that influence PINK1 abundance in the fruit fly Drosophila melanogaster. We found that genetic perturbations targeting the matrix-localized protease Lon caused dramatic accumulation of processed PINK1 species in several mitochondrial compartments, including the matrix. Knockdown of Lon did not decrease mitochondrial membrane potential or trigger activation of the mitochondrial unfolded protein stress response (UPRmt), indicating that PINK1 accumulation in Lon-deficient animals is not a secondary consequence of mitochondrial depolarization or the UPRmt. Moreover, the influence of Lon on PINK1 abundance was highly specific, as Lon inactivation had little or no effect on the abundance of other mitochondrial proteins. Further studies indicated that the processed forms of PINK1 that accumulate upon Lon inactivation are capable of activating the PINK1-Parkin pathway in vivo. Our findings thus suggest that Lon plays an essential role in regulating the PINK1-Parkin pathway by promoting the degradation of PINK1 in the matrix of healthy mitochondria.