The Price Premium for Organic Babyfood: A Hedonic Analysis

The price premium associated with organic babyfood is estimated by applying a hedonic model to price and characteristic data for babyfood products collected in two cities: Raleigh, North Carolina, and San Jose, California. The price per ounce of babyfood is modeled as a function of a number of babyfood and store characteristics. The estimated organic price premium is generally equal to 3 cents to 4 cents per ounce. To the extent this premium reflects consumer willingness to pay to reduce pesticide exposures, it could be used to infer values for reduced dietary exposures to pesticide residues for babies.babyfood, hedonic analysis, organic foods, Demand and Price Analysis,

WILL FARMERS USE SAFER PESTICIDES?

Virtually all technology adoption studies are conducted ex post, yet policy makers often need to assess the likely level of adoption before the technology is introduced. This study uses data from a contingent valuation survey of Michigan corn growers to assess what factors would influence the adoption of two safer corn herbicides, one that is not carcinogenic and one that does not leach. Results indicate that price, risk perception, and sources of pest control information are all important. This suggests that public policies designed to change perceptions and improve information dissemination may encourage voluntary use of more environmentally friendly technologies.atrazine, cancer risk, contingent valuation, herbicides, nitrate leaching, public policy, technology adoption, Crop Production/Industries,

CowN Sustains Nitrogenase Turnover in the Presence of the Inhibitor Carbon Monoxide

Nitrogenase is the only enzyme capable of catalyzing nitrogen fixation, the reduction of dinitrogen gas (N2) to ammonia (NH3). Nitrogenase is tightly inhibited by the environmental gas carbon monoxide (CO). Nitrogen-fixing bacteria rely on the protein CowN to grow in the presence of CO. However, the mechanism by which CowN operates is unknown. Here, we present the biochemical characterization of CowN and examine how CowN protects nitrogenase from CO. We determine that CowN interacts directly with nitrogenase and that CowN protection observes hyperbolic kinetics with respect to CowN concentration. At a CO concentration of 0.001 atm, CowN restores nearly full nitrogenase activity. Our results further indicate that CowN’s protection mechanism involves decreasing the binding affinity of CO to nitrogenase’s active site approximately tenfold without interrupting substrate turnover. Taken together, our work suggests CowN is an important auxiliary protein in nitrogen fixation that engenders CO tolerance to nitrogenase

COOL-LAMPS. VI. Lens Model and New Constraints on the Properties of COOL J1241+2219, a Bright z = 5 Lyman Break Galaxy and its z = 1 Cluster Lens

We present a strong lensing analysis of COOL J1241+2219, the brightest known gravitationally lensed galaxy at z ≥ 5, based on new multiband Hubble Space Telescope (HST) imaging data. The lensed galaxy has a redshift of z = 5.043, placing it shortly after the end of the “Epoch of Reionization,” and an AB magnitude z AB = 20.47 mag (Khullar et al.). As such, it serves as a touchstone for future research of that epoch. The high spatial resolution of HST reveals internal structure in the giant arc, from which we identify 15 constraints and construct a robust lens model. We use the lens model to extract the cluster mass and lensing magnification. We find that the mass enclosed within the Einstein radius of the z = 1.001 cluster lens is M(<5.″77)=1.079−0.007+0.023×1013M☉ , significantly lower than other known strong lensing clusters at its redshift. The average magnification of the giant arc is 〈μ arc〉 = 76−20+40 , a factor of 2.4−0.7+1.4 greater than previously estimated from ground-based data; the flux-weighted average magnification is 〈μ arc〉 = 92−31+37 . We update the current measurements of the stellar mass and star formation rate (SFR) of the source for the revised magnification to log(M⋆/M⊙)= 9.7 ± 0.3 and SFR = 10.3−4.4+7.0 M ⊙ yr−1, respectively. The powerful lensing magnification acting upon COOL J1241+2219 resolves the source and enables future studies of the properties of its star formation on a clump-by-clump basis. The lensing analysis presented here will support upcoming multiwavelength characterization with HST and JWST data of the stellar mass assembly and physical properties of this high-redshift lensed galaxy

COOL-LAMPS VI: Lens model and New Constraints on the Properties of COOL J1241+2219, a Bright z = 5 Lyman Break Galaxy and its z = 1 Cluster Lens

We present a strong lensing analysis of COOL J1241+2219, the brightest known gravitationally lensed galaxy at $z \geq 5$, based on new multi-band Hubble Space Telescope (HST) imaging data. The lensed galaxy has a redshift of z=5.043, placing it shortly after the end of the Epoch of Reionization, and an AB magnitude z_AB=20.47 mag (Khullar et al. 2021). As such, it serves as a touchstone for future research of that epoch. The high spatial resolution of HST reveals internal structure in the giant arc, from which we identify 15 constraints and construct a robust lens model. We use the lens model to extract cluster mass and lensing magnification. We find that the mass enclosed within the Einstein radius of the z=1.001 cluster lens is M(<5.77'')=$1.079^{+0.023}_{-0.007}$, significantly lower than other known strong lensing clusters at its redshift. The average magnification of the giant arc is $=76^{+40}_{-20}$, a factor of $2.4^{+1.4}_{-0.7}$ greater than previously estimated from ground-based data; the flux-weighted average magnification is $=92^{+37}_{-31}$ We update the current measurements of the stellar mass and star formation rate (SFR) of the source for the revised magnification, $\log(M_\star/M_{\odot})=9.7\pm0.3$ and ${\rm SFR} = 10.3^{+7.0}_{-4.4}$ $M_{\odot}$yr$^{-1}$. The powerful lensing magnification acting upon COOL J1241+2219 resolves the source and enables future studies of the properties of its star formation on a clump-by-clump basis. The lensing analysis presented here will support upcoming multiwavelength characterization with HST and JWST data of the stellar mass assembly and physical properties of this high-redshift lensed galaxy.Comment: Submitted to Ap

Pathogenetics of alveolar capillary dysplasia with misalignment of pulmonary veins.

Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a lethal lung developmental disorder caused by heterozygous point mutations or genomic deletion copy-number variants (CNVs) of FOXF1 or its upstream enhancer involving fetal lung-expressed long noncoding RNA genes LINC01081 and LINC01082. Using custom-designed array comparative genomic hybridization, Sanger sequencing, whole exome sequencing (WES), and bioinformatic analyses, we studied 22 new unrelated families (20 postnatal and two prenatal) with clinically diagnosed ACDMPV. We describe novel deletion CNVs at the FOXF1 locus in 13 unrelated ACDMPV patients. Together with the previously reported cases, all 31 genomic deletions in 16q24.1, pathogenic for ACDMPV, for which parental origin was determined, arose de novo with 30 of them occurring on the maternally inherited chromosome 16, strongly implicating genomic imprinting of the FOXF1 locus in human lungs. Surprisingly, we have also identified four ACDMPV families with the pathogenic variants in the FOXF1 locus that arose on paternal chromosome 16. Interestingly, a combination of the severe cardiac defects, including hypoplastic left heart, and single umbilical artery were observed only in children with deletion CNVs involving FOXF1 and its upstream enhancer. Our data demonstrate that genomic imprinting at 16q24.1 plays an important role in variable ACDMPV manifestation likely through long-range regulation of FOXF1 expression, and may be also responsible for key phenotypic features of maternal uniparental disomy 16. Moreover, in one family, WES revealed a de novo missense variant in ESRP1, potentially implicating FGF signaling in the etiology of ACDMPV

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

The James Webb Space Telescope Mission

Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least $4m$. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the $6.5m$ James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure