Estimating implicit and explicit gender bias among health care professionals and surgeons

Importance: The Implicit Association Test (IAT) is a validated tool used to measure implicit biases, which are mental associations shaped by one\u27s environment that influence interactions with others. Direct evidence of implicit gender biases about women in medicine has yet not been reported, but existing evidence is suggestive of subtle or hidden biases that affect women in medicine. Objectives: To use data from IATs to assess (1) how health care professionals associate men and women with career and family and (2) how surgeons associate men and women with surgery and family medicine. Design, Setting, and Participants: This data review and cross-sectional study collected data from January 1, 2006, through December 31, 2017, from self-identified health care professionals taking the Gender-Career IAT hosted by Project Implicit to explore bias among self-identified health care professionals. A novel Gender-Specialty IAT was also tested at a national surgical meeting in October 2017. All health care professionals who completed the Gender-Career IAT were eligible for the first analysis. Surgeons of any age, gender, title, and country of origin at the meeting were eligible to participate in the second analysis. Data were analyzed from January 1, 2018, through March 31, 2019. Main Outcomes and Measures: Measure of implicit bias derived from reaction times on the IATs and a measure of explicit bias asked directly to participants. Results: Almost 1 million IAT records from Project Implicit were reviewed, and 131 surgeons (64.9% men; mean [SD] age, 42.3 [11.5] years) were recruited to complete the Gender-Specialty IAT. Healthcare professionals (n = 42 991; 82.0% women; mean [SD] age, 32.7 [11.8] years) held implicit (mean [SD] D score, 0.41 [0.36]; Cohen d = 1.14) and explicit (mean [SD], 1.43 [1.85]; Cohen d = 0.77) biases associating men with career and women with family. Similarly, surgeons implicitly (mean [SD] D score, 0.28 [0.37]; Cohen d = 0.76) and explicitly (men: mean [SD], 1.27 [0.39]; Cohen d = 0.93; women: mean [SD], 0.73 [0.35]; Cohen d = 0.53) associated men with surgery and women with family medicine. There was broad evidence of consensus across social groups in implicit and explicit biases with one exception. Women in healthcare (mean [SD], 1.43 [1.86]; Cohen d = 0.77) and surgery (mean [SD], 0.73 [0.35]; Cohen d = 0.53) were less likely than men to explicitly associate men with career (B coefficient, -0.10; 95% CI, -0.15 to -0.04; P \u3c .001) and surgery (B coefficient, -0.67; 95% CI, -1.21 to -0.13; P = .001) and women with family and family medicine. Conclusions and Relevance: The main contribution of this work is an estimate of the extent of implicit gender bias within surgery. On both the Gender-Career IAT and the novel Gender-Specialty IAT, respondents had a tendency to associate men with career and surgery and women with family and family medicine. Awareness of the existence of implicit biases is an important first step toward minimizing their potential effect

Heterogeneity in Surface Sensing Suggests a Division of Labor in Pseudomonas aeruginosa Populations

The second messenger signaling molecule cyclic diguanylate monophosphate (c-di-GMP) drives the transition between planktonic and biofilm growth in many bacterial species. Pseudomonas aeruginosa has two surface sensing systems that produce c-di-GMP in response to surface adherence. Current thinking in the field is that once cells attach to a surface, they uniformly respond by producing c-di-GMP. Here, we describe how the Wsp system generates heterogeneity in surface sensing, resulting in two physiologically distinct subpopulations of cells. One subpopulation has elevated c-di-GMP and produces biofilm matrix, serving as the founders of initial microcolonies. The other subpopulation has low c-di-GMP and engages in surface motility, allowing for exploration of the surface. We also show that this heterogeneity strongly correlates to surface behavior for descendent cells. Together, our results suggest that after surface attachment, P. aeruginosa engages in a division of labor that persists across generations, accelerating early biofilm formation and surface exploration

Common Genetic Variants Explain the Majority of the Correlation Between Height and Intelligence : The Generation Scotland Study

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c-di-GMP modulates type IV MSHA pilus retraction and surface attachment in Vibrio cholerae.

Biofilm formation by Vibrio cholerae facilitates environmental persistence, and hyperinfectivity within the host. Biofilm formation is regulated by 3',5'-cyclic diguanylate (c-di-GMP) and requires production of the type IV mannose-sensitive hemagglutinin (MSHA) pilus. Here, we show that the MSHA pilus is a dynamic extendable and retractable system, and its activity is directly controlled by c-di-GMP. The interaction between c-di-GMP and the ATPase MshE promotes pilus extension, whereas low levels of c-di-GMP correlate with enhanced retraction. Loss of retraction facilitated by the ATPase PilT increases near-surface roaming motility, and impairs initial surface attachment. However, prolonged retraction upon surface attachment results in reduced MSHA-mediated surface anchoring and increased levels of detachment. Our results indicate that c-di-GMP directly controls MshE activity, thus regulating MSHA pilus extension and retraction dynamics, and modulating V. cholerae surface attachment and colonization

Quasi 3D ECE imaging system for study of MHD instabilities in KSTAR

A second electron cyclotron emission imaging (ECEI) system has been installed on the KSTAR tokamak, toroidally separated by 1/16th of the torus from the first ECEI system. For the first time, the dynamical evolutions of MHD instabilities from the plasma core to the edge have been visualized in quasi-3D for a wide range of the KSTAR operation (B0 = 1.7???3.5 T). This flexible diagnostic capability has been realized by substantial improvements in large-aperture quasi-optical microwave components including the development of broad-band polarization rotators for imaging of the fundamental ordinary ECE as well as the usual 2nd harmonic extraordinary ECE.open1

Allelic Variation on Murine Chromosome 11 Modifies Host Inflammatory Responses and Resistance to Bacillus anthracis

Anthrax is a potentially fatal disease resulting from infection with Bacillus anthracis. The outcome of infection is influenced by pathogen-encoded virulence factors such as lethal toxin (LT), as well as by genetic variation within the host. To identify host genes controlling susceptibility to anthrax, a library of congenic mice consisting of strains with homozygous chromosomal segments from the LT-responsive CAST/Ei strain introgressed on a LT-resistant C57BL/6 (B6) background was screened for response to LT. Three congenic strains containing CAST/Ei regions of chromosome 11 were identified that displayed a rapid inflammatory response to LT similar to, but more severe than that driven by a LT-responsive allele of the inflammasome constituent NRLP1B. Importantly, increased response to LT in congenic mice correlated with greater resistance to infection by the Sterne strain of B. anthracis. The genomic region controlling the inflammatory response to LT was mapped to 66.36–74.67 Mb on chromosome 11, a region that encodes the LT-responsive CAST/Ei allele of Nlrp1b. However, known downstream effects of NLRP1B activation, including macrophage pyroptosis, cytokine release, and leukocyte infiltration could not fully explain the response to LT or the resistance to B. anthracis Sterne in congenic mice. Further, the exacerbated response in congenic mice is inherited in a recessive manner while the Nlrp1b-mediated response to LT is dominant. Finally, congenic mice displayed increased responsiveness in a model of sepsis compared with B6 mice. In total, these data suggest that allelic variation of one or more chromosome 11 genes in addition to Nlrp1b controls the severity of host response to multiple inflammatory stimuli and contributes to resistance to B. anthracis Sterne. Expression quantitative trait locus analysis revealed 25 genes within this region as high priority candidates for contributing to the host response to LT

Supramolecular assemblies involving metal organic ring interactions: Heterometallic Cu(II)-Ln(III) two dimensional coordination polymers

Three isostructural two-dimensional coordination polymers of the general formula [Ln2(CuL)3(H2O)9]$5.5H2O, where Ln is La (1), Nd (2), and Gd (3), have been synthesized and isolated from aqueous solutions and their single-crystal structures determined by X-ray diffraction. The supramolecular interaction between the non-aromatic metallorings plays an important role in stabilizing the structure of these compounds. The thermal stability, reversible solvent uptake, electronic properties and magnetic studies of these compounds are also reported

Extracellular Myocardial Volume in Patients With Aortic Stenosis

BACKGROUND: Myocardial fibrosis is a key mechanism of left ventricular decompensation in aortic stenosis and can be quantified using cardiovascular magnetic resonance (CMR) measures such as extracellular volume fraction (ECV%). Outcomes following aortic valve intervention may be linked to the presence and extent of myocardial fibrosis. OBJECTIVES: This study sought to determine associations between ECV% and markers of left ventricular decompensation and post-intervention clinical outcomes. METHODS: Patients with severe aortic stenosis underwent CMR, including ECV% quantification using modified Look-Locker inversion recovery-based T1 mapping and late gadolinium enhancement before aortic valve intervention. A central core laboratory quantified CMR parameters. RESULTS: Four-hundred forty patients (age 70 ± 10 years, 59% male) from 10 international centers underwent CMR a median of 15 days (IQR: 4 to 58 days) before aortic valve intervention. ECV% did not vary by scanner manufacturer, magnetic field strength, or T1 mapping sequence (all p > 0.20). ECV% correlated with markers of left ventricular decompensation including left ventricular mass, left atrial volume, New York Heart Association functional class III/IV, late gadolinium enhancement, and lower left ventricular ejection fraction (p < 0.05 for all), the latter 2 associations being independent of all other clinical variables (p = 0.035 and p < 0.001). After a median of 3.8 years (IQR: 2.8 to 4.6 years) of follow-up, 52 patients had died, 14 from adjudicated cardiovascular causes. A progressive increase in all-cause mortality was seen across tertiles of ECV% (17.3, 31.6, and 52.7 deaths per 1,000 patient-years; log-rank test; p = 0.009). Not only was ECV% associated with cardiovascular mortality (p = 0.003), but it was also independently associated with all-cause mortality following adjustment for age, sex, ejection fraction, and late gadolinium enhancement (hazard ratio per percent increase in ECV%: 1.10; 95% confidence interval [1.02 to 1.19]; p = 0.013). CONCLUSIONS: In patients with severe aortic stenosis scheduled for aortic valve intervention, an increased ECV% is a measure of left ventricular decompensation and a powerful independent predictor of mortality

Structural and functional basis for RNA cleavage by Ire1

BACKGROUND: The unfolded protein response (UPR) controls the protein folding capacity of the endoplasmic reticulum (ER). Central to this signaling pathway is the ER-resident bifunctional transmembrane kinase/endoribonuclease Ire1. The endoribonuclease (RNase) domain of Ire1 initiates a non-conventional mRNA splicing reaction, leading to the production of a transcription factor that controls UPR target genes. The mRNA splicing reaction is an obligatory step of Ire1 signaling, yet its mechanism has remained poorly understood due to the absence of substrate-bound crystal structures of Ire1, the lack of structural similarity between Ire1 and other RNases, and a scarcity of quantitative enzymological data. Here, we experimentally define the active site of Ire1 RNase and quantitatively evaluate the contribution of the key active site residues to catalysis. RESULTS: This analysis and two new crystal structures suggest that Ire1 RNase uses histidine H1061 and tyrosine Y1043 as the general acid-general base pair contributing \u3e/=7.6 kcal/mol and 1.4 kcal/mol to transition state stabilization, respectively, and asparagine N1057 and arginine R1056 for coordination of the scissile phosphate. Investigation of the stem-loop recognition revealed that additionally to the stem-loops derived from the classic Ire1 substrates HAC1 and Xbp1 mRNA, Ire1 can site-specifically and rapidly cleave anticodon stem-loop (ASL) of unmodified tRNAPhe, extending known substrate specificity of Ire1 RNase. CONCLUSIONS: Our data define the catalytic center of Ire1 RNase and suggest a mechanism of RNA cleavage: each RNase monomer apparently contains a separate catalytic apparatus for RNA cleavage, whereas two RNase subunits contribute to RNA stem-loop docking. Conservation of the key residues among Ire1 homologues suggests that the mechanism elucidated here for yeast Ire1 applies to Ire1 in metazoan cells, and to the only known Ire1 homologue RNase L