Miracle-dz/UniFAR-FTUs huggingface dataset:
Effect of Prehospital Red Blood Cell Transfusion on Mortality and Time of Death in Civilian Trauma Patients

Background: Current management principles of hemorrhagic shock after trauma emphasize earlier transfusion therapy to prevent dilution of clotting factors and correct coagulopathy. London's Air Ambulance (LAA) was the first UK civilian prehospital service to routinely offer prehospital red blood cell (RBC) transfusion (phRTx). We investigated the effect of phRTx on mortality. Methods: Retrospective trauma database study comparing mortality before implementation with after implementation of phRTx in exsanguinating trauma patients. Univariate logistic regression was performed for the unadjusted association between phRTx and mortality was performed, and multiple logistic regression adjusting for potential confounders. Results: We identified 623 subjects with suspected major hemorrhage. We excluded 84 (13.5%) patients due to missing data on survival status. Overall 187 (62.3%) patients died in the before phRTx period and 143 (59.8%) died in the after phRTx group. There was no significant improvement in overall survival after the introduction of phRTx (P = 0.554). Examination of prehospital mortality demonstrated 126 deaths in the pre-phRTx group (42.2%) and 66 deaths in the RBC administered group (27.6%). There was a significant reduction in prehospital mortality in the group who received RBC (P < 0.001). Conclusions: phRTx was associated with increased survival to hospital, but not overall survival. The “delay death” effect of phRTx carries an impetus to further develop inhospital strategies to improve survival in severely bleeding patients.
Role of miR‐31 and SATB2 in arsenic‐induced malignant BEAS‐2B cell transformation

Arsenic is a naturally occurring and highly potent metalloid known to elicit serious public health concerns. Today, approximately 200 million people around the globe are exposed to arsenic‐contaminated drinking water at levels greater than the World Health Organization's recommended limit of 10 parts per billion. As a class I human carcinogen, arsenic exposure is known to elicit various cancers, including lung, skin, liver, and kidney. Current evidence suggests that arsenic is capable of inducing both genotoxic and cytotoxic injury, as well as activating epigenetic pathways to induce carcinogenesis. Our study identifies a novel pathway that is implicated in arsenic‐induced carcinogenesis. Arsenic down‐regulated miRNA‐31 and the release of this inhibition caused overexpression of special AT‐rich sequence‐binding protein 2 (SATB2). Arsenic is known to disrupt miRNA expression, and here we report for the first time that arsenic is capable of inhibiting miR‐31 expression. As a direct downstream target of miR‐31, SATB2 is a prominent transcription factor, and nuclear matrix binding protein implicated in many types of human diseases including lung cancer. Results from this study show that arsenic induces the overexpressing SATB2 by inhibiting miR‐31 expression, which blocks the translation of SATB2 mRNA, since levels of SATB2 mRNA remain the same but protein levels decrease. Overexpression of SATB2 induces malignant transformation of human bronchial epithelial (BEAS‐2B) cells indicating the importance of the expression of miR‐31 in preventing carcinogenesis by suppressing SATB2 protein levels.
Different indices of fetal growth predict bone size and volumetric density at 4 years of age

We have demonstrated previously that higher birth weight is associated with greater peak and later‐life bone mineral content and that maternal body build, diet, and lifestyle influence prenatal bone mineral accrual. To examine prenatal influences on bone health further, we related ultrasound measures of fetal growth to childhood bone size and density. We derived Z‐scores for fetal femur length and abdominal circumference and conditional growth velocity from 19 to 34 weeks' gestation from ultrasound measurements in participants in the Southampton Women's Survey. A total of 380 of the offspring underwent dual‐energy X‐ray absorptiometry (DXA) at age 4 years [whole body minus head bone area (BA), bone mineral content (BMC), areal bone mineral density (aBMD), and estimated volumetric BMD (vBMD)]. Volumetric bone mineral density was estimated using BMC adjusted for BA, height, and weight. A higher velocity of 19‐ to 34‐week fetal femur growth was strongly associated with greater childhood skeletal size (BA: r = 0.30, p < .0001) but not with volumetric density (vBMD: r = 0.03, p = .51). Conversely, a higher velocity of 19‐ to 34‐week fetal abdominal growth was associated with greater childhood volumetric density (vBMD: r = 0.15, p = .004) but not with skeletal size (BA: r = 0.06, p = .21). Both fetal measurements were positively associated with BMC and aBMD, indices influenced by both size and density. The velocity of fetal femur length growth from 19 to 34 weeks' gestation predicted childhood skeletal size at age 4 years, whereas the velocity of abdominal growth (a measure of liver volume and adiposity) predicted volumetric density. These results suggest a discordance between influences on skeletal size and volumetric density. © 2010 American Society for Bone and Mineral Research
Proton Pump Inhibitors and Serum Magnesium Levels in Patients With Torsades de Pointes

Background: Torsades de pointes (TdP) is a life-threatening ventricular tachycardia occurring in long QT-syndrome patients. It usually develops when multiple QT-prolonging factors are concomitantly present, more frequently drugs and electrolyte imbalances. Since proton–pump inhibitors (PPIs)-associated hypomagnesemia is an increasingly recognized adverse event, PPIs were recently included in the list of drugs with conditional risk of TdP, despite only few cases of TdP in PPI users have been reported so far. Objectives: Aim of the present study is to evaluate whether PPI-induced hypomagnesemia actually has a significant clinical impact on the risk of TdP in the general population. Methods: Forty-eight unselected patients who experienced TdP were consecutively enrolled (2008-2017). Shortly after the first TdP episode, in those patients who did not receive magnesium sulfate and/or potassium or calcium replacement therapy, serum electrolytes were measured and their relationship with PPI usage analyzed. Results: Many patients (28/48, 58%) were under current PPI treatment when TdP occurred. Among TdP patients in whom serum electrolyte determinations were obtained before replacement therapy (27/48), those taking PPIs had significantly lower serum magnesium levels than those who did not. Hypomagnesemia occurred in ~40% of patients receiving PPIs (6/14), in all cases after an extended treatment (>2 weeks). In patients taking PPIs the mean QT-prolonging risk factor number was significantly higher than in those who did not, a difference which was mainly driven by lower magnesium levels. Conclusions: In unselected TdP patients, PPI-induced hypomagnesemia was common and significantly contributed to their cumulative arrhythmic risk. By providing clinical support to current recommendations, our data confirm that more awareness is needed when a PPI is prescribed, specifically as regards the risk of life-threatening arrhythmias.
Mechanosensitivity of Jagged–Notch signaling can induce a switch-type behavior in vascular homeostasis

Significance Notch signaling and hemodynamics are widely known to regulate arterial morphogenesis, remodeling, and homeostasis. Recent studies suggest that Notch signaling and mechanics interact in vascular remodeling, but the impact on vascular homeostasis is still unclear. Here, using a computational–experimental approach, we show that expression of Notch ligands, receptors, and target genes are down-regulated with mechanical strain. Incorporation of these results in a computational model of the arterial wall reveals that this mechanosensitivity leads to a sudden transition from synthetic toward contractile smooth muscle cells at a certain wall thickness, which varies per arterial location and closely agrees with reported anatomical data. This result provides an explanation for how mechanical forces can regulate arterial morphogenesis and homeostasis through Notch signaling. Hemodynamic forces and Notch signaling are both known as key regulators of arterial remodeling and homeostasis. However, how these two factors integrate in vascular morphogenesis and homeostasis is unclear. Here, we combined experiments and modeling to evaluate the impact of the integration of mechanics and Notch signaling on vascular homeostasis. Vascular smooth muscle cells (VSMCs) were cyclically stretched on flexible membranes, as quantified via video tracking, demonstrating that the expression of Jagged1, Notch3, and target genes was down-regulated with strain. The data were incorporated in a computational framework of Notch signaling in the vascular wall, where the mechanical load was defined by the vascular geometry and blood pressure. Upon increasing wall thickness, the model predicted a switch-type behavior of the Notch signaling state with a steep transition of synthetic toward contractile VSMCs at a certain transition thickness. These thicknesses varied per investigated arterial location and were in good agreement with human anatomical data, thereby suggesting that the Notch response to hemodynamics plays an important role in the establishment of vascular homeostasis.
Topological order in the pseudogap metal

Significance The copper oxide-based high-temperature superconductors display a mysterious “pseudogap” metal phase at temperatures just above the critical temperature in a regime of low hole density. Extensive experimental and numerical studies have yielded much information on the nature of the electron corrections, but a fundamental theoretical understanding has been lacking. We show that a theory of a metal with topological order and emergent gauge fields can model much of the numerical data. Our study opens up a route to a deeper understanding of the long-range quantum entanglement in these superconductors and to the direct detection of the topological characteristics of the many-body quantum state. We compute the electronic Green’s function of the topologically ordered Higgs phase of a SU(2) gauge theory of fluctuating antiferromagnetism on the square lattice. The results are compared with cluster extensions of dynamical mean field theory, and quantum Monte Carlo calculations, on the pseudogap phase of the strongly interacting hole-doped Hubbard model. Good agreement is found in the momentum, frequency, hopping, and doping dependencies of the spectral function and electronic self-energy. We show that lines of (approximate) zeros of the zero-frequency electronic Green’s function are signs of the underlying topological order of the gauge theory and describe how these lines of zeros appear in our theory of the Hubbard model. We also derive a modified, nonperturbative version of the Luttinger theorem that holds in the Higgs phase.
Local Descriptors Optimized for Average Precision

Extraction of local feature descriptors is a vital stage in the solution pipelines for numerous computer vision tasks. Learning-based approaches improve performance in certain tasks, but still cannot replace handcrafted features in general. In this paper, we improve the learning of local feature descriptors by optimizing the performance of descriptor matching, which is a common stage that follows descriptor extraction in local feature based pipelines, and can be formulated as nearest neighbor retrieval. Specifically, we directly optimize a ranking-based retrieval performance metric, Average Precision, using deep neural networks. This general-purpose solution can also be viewed as a listwise learning to rank approach, which is advantageous compared to recent local ranking approaches. On standard benchmarks, descriptors learned with our formulation achieve state-of-the-art results in patch verification, patch retrieval, and image matching,
Seagrass habitat metabolism increases short-term extremes and long-term offset of CO2 under future ocean acidification

Significance The impacts of ocean acidification in nearshore estuarine environments remain poorly characterized, despite these areas being some of the most ecologically important habitats in the global ocean. Here, we quantify how rising atmospheric CO2 from the years 1765 to 2100 alters high-frequency carbonate chemistry dynamics in an estuarine seagrass habitat. We find that increasing anthropogenic carbon reduces the ability of the system to buffer natural extremes in CO2. This reduced buffering capacity leads to preferential amplification of naturally extreme low pH and high pCO2(s.w.) events above changes in average conditions, which outpace rates published for atmospheric and open-ocean CO2 change. Seagrass habitat metabolism drives these short-term extreme events, yet ultimately reduces organismal exposure to harmful conditions in future high-CO2 scenarios. The role of rising atmospheric CO2 in modulating estuarine carbonate system dynamics remains poorly characterized, likely due to myriad processes driving the complex chemistry in these habitats. We reconstructed the full carbonate system of an estuarine seagrass habitat for a summer period of 2.5 months utilizing a combination of time-series observations and mechanistic modeling, and quantified the roles of aerobic metabolism, mixing, and gas exchange in the observed dynamics. The anthropogenic CO2 burden in the habitat was estimated for the years 1765–2100 to quantify changes in observed high-frequency carbonate chemistry dynamics. The addition of anthropogenic CO2 alters the thermodynamic buffer factors (e.g., the Revelle factor) of the carbonate system, decreasing the seagrass habitat’s ability to buffer natural carbonate system fluctuations. As a result, the most harmful carbonate system indices for many estuarine organisms [minimum pHT, minimum Ωarag, and maximum pCO2(s.w.)] change up to 1.8×, 2.3×, and 1.5× more rapidly than the medians for each parameter, respectively. In this system, the relative benefits of the seagrass habitat in locally mitigating ocean acidification increase with the higher atmospheric CO2 levels predicted toward 2100. Presently, however, these mitigating effects are mixed due to intense diel cycling of CO2 driven by aerobic metabolism. This study provides estimates of how high-frequency pHT, Ωarag, and pCO2(s.w.) dynamics are altered by rising atmospheric CO2 in an estuarine habitat, and highlights nonlinear responses of coastal carbonate parameters to ocean acidification relevant for water quality management.
GSK-3Beta-Dependent Activation of GEF-H1/ROCK Signaling Promotes LPS-Induced Lung Vascular Endothelial Barrier Dysfunction and Acute Lung Injury

The bacterial endotoxin or lipopolysaccharide (LPS) leads to the extensive vascular endothelial cells (EC) injury under septic conditions. Guanine nucleotide exchange factor-H1 (GEF-H1)/ROCK signaling not only involved in LPS-induced overexpression of pro-inflammatory mediator in ECs but also implicated in LPS-induced endothelial hyper-permeability. However, the mechanisms behind LPS-induced GEF-H1/ROCK signaling activation in the progress of EC injury remain incompletely understood. GEF-H1 localized on microtubules (MT) and is suppressed in its MT-bound state. MT disassembly promotes GEF-H1 release from MT and stimulates downstream ROCK-specific GEF activity. Since glycogen synthase kinase (GSK-3beta) participates in regulating MT dynamics under pathologic conditions, we examined the pivotal roles for GSK-3beta in modulating LPS-induced activation of GEF-H1/ROCK, increase of vascular endothelial permeability and severity of acute lung injury (ALI). In this study, we found that LPS induced human pulmonary endothelial cell (HPMEC) monolayers disruption accompanied by increase in GSK-3beta activity, activation of GEF-H1/ROCK signaling and decrease in beta-catenin and ZO-1 expression. Inhibition of GSK-3beta reduced HPMEC monolayers hyper-permeability and GEF-H1/ROCK activity in response to LPS. GSK-3beta/GEF-H1/ROCK signaling is implicated in regulating the expression of beta-catenin and ZO-1. In vivo, GSK-3beta inhibition attenuated LPS-induced activation of GEF-H1/ROCK pathway, lung edema and subsequent ALI. These findings present a new mechanism of GSK-3beta-dependent exacerbation of lung micro-vascular hyper-permeability and escalation of ALI via activation of GEF-H1/ROCK signaling and disruption of intracellular junctional proteins under septic condition.
Formation Control of Nonholonomic Mobile Robots Without Position and Velocity Measurements

Most existing formation control approaches are based on the assumption that the global/relative position and/or velocity measurements of mobile robots are directly available. To extend the application domain and to improve the formation control performance, it is extremely necessary to avoid the use of position and velocity measurements in the design of formation controllers. In this paper, we propose new leader-following formation tracking control schemes for nonholonomic mobile robots with onboard perspective cameras, without using both position and velocity measurements. To address the unavailability issue of position measurements, the leader–follower kinematics model in the image space is developed, which can facilitate the complete elimination of measurement/estimation of the position information. Furthermore, feedback information from the perspective camera of the follower robot is used to design adaptive observers to estimate the leader linear velocity for feedforward compensation, which can handle the absence of velocity measurements such that the proposed schemes can be applied to control formations of mobile robots without mutual communication abilities. By using the Lyapunov stability theory, a rigorous stability analysis based on the nonlinear formation dynamics is provided to show that the global stability of the combined observer–controller closed-loop system can be guaranteed. Both simulation and experimental results are also given to demonstrate the performance of the proposed formation tracking control schemes.
Hip extensor mechanics and the evolution of walking and climbing capabilities in humans, apes, and fossil hominins

Significance The evolution of humans’ distinct bipedal gait remains a focus of research and debate. Many reconstructions of hominin locomotor evolution assume climbing capability trades off against walking economy, with improvement in one requiring diminishment of the other, but few have tested these functional inferences experimentally. In this study, we integrate experimental locomotor mechanics from humans and other primates with osteological measurements to assess the locomotor capabilities of early hominins. Our analyses show that changes in the ischium and hamstrings would have made walking more economical without reducing the utility of these muscles for climbing in early hominins. A wider set of evolutionary solutions may have been available to early hominins than previously recognized. The evolutionary emergence of humans’ remarkably economical walking gait remains a focus of research and debate, but experimentally validated approaches linking locomotor capability to postcranial anatomy are limited. In this study, we integrated 3D morphometrics of hominoid pelvic shape with experimental measurements of hip kinematics and kinetics during walking and climbing, hamstring activity, and passive range of hip extension in humans, apes, and other primates to assess arboreal–terrestrial trade-offs in ischium morphology among living taxa. We show that hamstring-powered hip extension during habitual walking and climbing in living apes and humans is strongly predicted, and likely constrained, by the relative length and orientation of the ischium. Ape pelves permit greater extensor moments at the hip, enhancing climbing capability, but limit their range of hip extension, resulting in a crouched gait. Human pelves reduce hip extensor moments but permit a greater degree of hip extension, which greatly improves walking economy (i.e., distance traveled/energy consumed). Applying these results to fossil pelves suggests that early hominins differed from both humans and extant apes in having an economical walking gait without sacrificing climbing capability. Ardipithecus was capable of nearly human-like hip extension during bipedal walking, but retained the capacity for powerful, ape-like hip extension during vertical climbing. Hip extension capability was essentially human-like in Australopithecus afarensis and Australopithecus africanus, suggesting an economical walking gait but reduced mechanical advantage for powered hip extension during climbing.
Effects of iron on the lattice thermal conductivity of Earth’s deep mantle and implications for mantle dynamics

Significance Presence of iron in Earth’s lower mantle may critically affect its physical properties and thermochemical structures. However, its effects on thermal conductivity and dynamics of deep mantle remain unknown. We studied lattice thermal conductivity of lower-mantle ferropericlase to 120 GPa using ultrafast optics. We observed an enhanced iron substitution effect in the low-spin iron-rich ferropericlase, with thermal conductivity that significantly drops across spin transition. Combined with bridgmanite data, we provided a self-consistent radial profile of lower-mantle thermal conductivity, which is dominated by pressure, temperature, and iron effects and shows a twofold increase throughout the lower mantle. If ultralow velocity zones are hot and strongly enriched in iron, their exceptionally low thermal conductivity will delay their cooling, influencing lowermost mantle dynamics. Iron may critically influence the physical properties and thermochemical structures of Earth’s lower mantle. Its effects on thermal conductivity, with possible consequences on heat transfer and mantle dynamics, however, remain largely unknown. We measured the lattice thermal conductivity of lower-mantle ferropericlase to 120 GPa using the ultrafast optical pump-probe technique in a diamond anvil cell. The thermal conductivity of ferropericlase with 56% iron significantly drops by a factor of 1.8 across the spin transition around 53 GPa, while that with 8–10% iron increases monotonically with pressure, causing an enhanced iron substitution effect in the low-spin state. Combined with bridgmanite data, modeling of our results provides a self-consistent radial profile of lower-mantle thermal conductivity, which is dominated by pressure, temperature, and iron effects, and shows a twofold increase from top to bottom of the lower mantle. Such increase in thermal conductivity may delay the cooling of the core, while its decrease with iron content may enhance the dynamics of large low shear-wave velocity provinces. Our findings further show that, if hot and strongly enriched in iron, the seismic ultralow velocity zones have exceptionally low conductivity, thus delaying their cooling.