Deriving Verb Predicates By Clustering Verbs with Arguments

Hand-built verb clusters such as the widely used Levin classes (Levin, 1993) have proved useful, but have limited coverage. Verb classes automatically induced from corpus data such as those from VerbKB (Wijaya, 2016), on the other hand, can give clusters with much larger coverage, and can be adapted to specific corpora such as Twitter. We present a method for clustering the outputs of VerbKB: verbs with their multiple argument types, e.g. "marry(person, person)", "feel(person, emotion)." We make use of a novel low-dimensional embedding of verbs and their arguments to produce high quality clusters in which the same verb can be in different clusters depending on its argument type. The resulting verb clusters do a better job than hand-built clusters of predicting sarcasm, sentiment, and locus of control in tweets

Landscapes: One to One Show Card

Show card for Landscapes: One to One, featuring faculty professor Lyle Novinski. Texas Wesleyan University. January 21 - February 21, 2003.https://digitalcommons.udallas.edu/faculty_off_campus_02-03/1000/thumbnail.jp

Modeling of Breakdown-Limited Endurance in Spin-Transfer Torque Magnetic Memory under Pulsed Cycling Regime

Perpendicular spin-transfer torque (p-STT) magnetic memory is gaining increasing interest as a candidate for storage-class memory, embedded memory, and possible replacement of static/dynamic memory. All these applications require extended cycling endurance, which should be based on a solid understanding and accurate modeling of the endurance failure mechanisms in the p-STT device. This paper addresses cycling endurance of p-STT memory under pulsed electrical switching. We show that endurance is limited by the dielectric breakdown of the magnetic tunnel junction stack, and we model endurance lifetime by the physical mechanisms leading to dielectric breakdown. The model predicts STT endurance as a function of applied voltage, pulsewidth, pulse polarity, and delay time between applied pulses. The dependence of the endurance on sample area is finally discussed

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

Axisymmetric gravity currents in a porous medium

The release from a point source of relatively heavy fluid into a saturated porous medium above an impermeable boundary is considered. A theoretical relationship is compared with experimental data for the rate of propagation of the front of the resulting gravity current and its shape. A motivation of the study, the problem of carbon dioxide sequestration, is briefly discussed

Table 2 - CO2 accumulation parameters

An analytical solution to the equations describing the flow of a buoyant fluid released into a porous medium below a horizontal impermeable boundary is used to model the growth of CO2 accumulations beneath thin mudstone beds in the Utsira sand reservoir at Sleipner in the North Sea. Here supercritical CO2 has been injected at a rate of ab. 1 MT/yr since 1996 and imaged by time-lapse seismic data in 1999, 2001 and 2002. The CO2 rises as a narrow plume and is partially trapped by a number of thin mudstones before reaching the caprock to the reservoir. The radii of the individual layers of trapped CO2 increase as the square root of time since initiation as predicted by the modelling for constant input flux. However apparent negative initiation times for horizons low in the reservoir suggests that net input fluxes for these layers have decreased with time, most probably as the spreading layers have increased their leakage rates. Accumulation of CO2 in the layers higher in the reservoir was initiated up to 3 yr after injection started. Modelling of the thickness profiles across three of the higher layers suggests that their net input fluxes have increased with time. The observation that the central thicknesses of the deeper layers have remained approximately constant, or have slightly decreased since first imaged in 1999, is consistent with the model predictions that the central thickness is directly proportional to net input flux. However, estimates of the permeability of the reservoir from the rate of increase of the radii of the CO2 accumulations are an order of magnitude less than measured permeabilities on the reservoir sandstone. Permeabilities estimated from the modelling of layer thickness changes scatter in the same range. These discrepancies may arise from, 1) approximations in the model not being valid, 2) the measured permeabilities not being representative of the permeability for two-phase flow on the scale of the reservoir or, considered less likely, 3) that much less CO2 is being stored in the imaged CO2 accumulations than estimated from the seismic reflection profiles. The most probable cause of the discrepancy is that the relative permeability for the CO2 phase is significantly reduced at lower CO2 saturations