Who is NIL Leaving Out?: Challenges and Solutions for International Student-Athletes

The National Collegiate Athletic Association (NCAA) adopted name, image and likeness (NIL) legislation in July 2021. The expectation was for all NCAA student-athletes to have the opportunity to seek compensation for their NIL, but the reality is quite different. International student-athletes are not easily able to benefit from their NIL due to restrictions placed on off-campus work under the terms of their entrance visas to the United States. This paper explores the need for the NCAA, NCAA member institutions, and government agencies to re-evaluate policies in an effort to ensure all student-athletes have the right to profit off their NIL. It is crucial that the membership is aware of how international student-athletes are confined by student visa regulations. In order to create a fair and equitable experience for all student-athletes, the NCAA and athletic departments need to understand off-campus work regulations and exceptions for international student visas (F-1 visa). Additionally, there is a need to advocate for this specific sub-population of student-athletes. We explore the idea of creating the opportunity for NIL to be on considered on-campus work for international student-athletes, or perhaps even assisting this population in filing exceptions within the constructs of the law. With domestic student-athletes already benefiting from NIL, it is time to find ways to allow international student-athletes to do the same. In essence, such opportunities would create one less barrier for international student-athletes who already face difficulty adjusting to life in the US

Extensive Lensing Survey of Optical and Near-infrared Dark Objects (El Sonido): HST H-faint Galaxies behind 101 Lensing Clusters

We present a Spitzer/IRAC survey of H-faint (H160 ≳ 26.4, < 5σ) sources in 101 lensing cluster fields. Across a CANDELS/Wide-like survey area of ∼648 arcmin2 (effectively ∼221 arcmin2 in the source plane), we have securely discovered 53 sources in the IRAC Channel-2 band (CH2, 4.5 μm; median CH2 = 22.46 ± 0.11 AB mag) that lack robust HST/WFC3-IR F160W counterparts. The most remarkable source in our sample, namely ES-009 in the field of Abell 2813, is the brightest H-faint galaxy at 4.5 μm known so far (CH2 = 20.48 ± 0.03 AB mag). We show that the H-faint sources in our sample are massive (median Mstar = 1010.3±0.3 M⊙), star-forming (median star formation rate $={100}_{-40}^{+60}$ M⊙ yr−1), and dust-obscured (AV = 2.6 ± 0.3) galaxies around a median photometric redshift of z = 3.9 ± 0.4. The stellar continua of 14 H-faint galaxies can be resolved in the CH2 band, suggesting a median circularized effective radius (Re,circ; lensing corrected) of 1.9 ± 0.2 kpc and <1.5 kpc for the resolved and whole samples, respectively. This is consistent with the sizes of massive unobscured galaxies at z ∼ 4, indicating that H-faint galaxies represent the dusty tail of the distribution of a wider galaxy population. Comparing with the ALMA dust continuum sizes of similar galaxies reported previously, we conclude that the heavy dust obscuration in H-faint galaxies is related to the compactness of both stellar and dust continua (Re,circ ∼ 1 kpc). These H-faint galaxies make up ${16}_{-7}^{+13}$% of the galaxies in the stellar-mass range of 1010 − 1011.2 M⊙ at z = 3 ∼ 5, contributing to ${8}_{-4}^{+8}$% of the cosmic star formation rate density in this epoch and likely tracing the early phase of massive galaxy formatio

Atrasentan and renal events in patients with type 2 diabetes and chronic kidney disease (SONAR): a double-blind, randomised, placebo-controlled trial

Background: Short-term treatment for people with type 2 diabetes using a low dose of the selective endothelin A receptor antagonist atrasentan reduces albuminuria without causing significant sodium retention. We report the long-term effects of treatment with atrasentan on major renal outcomes. Methods: We did this double-blind, randomised, placebo-controlled trial at 689 sites in 41 countries. We enrolled adults aged 18–85 years with type 2 diabetes, estimated glomerular filtration rate (eGFR)25–75 mL/min per 1·73 m 2 of body surface area, and a urine albumin-to-creatinine ratio (UACR)of 300–5000 mg/g who had received maximum labelled or tolerated renin–angiotensin system inhibition for at least 4 weeks. Participants were given atrasentan 0·75 mg orally daily during an enrichment period before random group assignment. Those with a UACR decrease of at least 30% with no substantial fluid retention during the enrichment period (responders)were included in the double-blind treatment period. Responders were randomly assigned to receive either atrasentan 0·75 mg orally daily or placebo. All patients and investigators were masked to treatment assignment. The primary endpoint was a composite of doubling of serum creatinine (sustained for ≥30 days)or end-stage kidney disease (eGFR <15 mL/min per 1·73 m 2 sustained for ≥90 days, chronic dialysis for ≥90 days, kidney transplantation, or death from kidney failure)in the intention-to-treat population of all responders. Safety was assessed in all patients who received at least one dose of their assigned study treatment. The study is registered with ClinicalTrials.gov, number NCT01858532. Findings: Between May 17, 2013, and July 13, 2017, 11 087 patients were screened; 5117 entered the enrichment period, and 4711 completed the enrichment period. Of these, 2648 patients were responders and were randomly assigned to the atrasentan group (n=1325)or placebo group (n=1323). Median follow-up was 2·2 years (IQR 1·4–2·9). 79 (6·0%)of 1325 patients in the atrasentan group and 105 (7·9%)of 1323 in the placebo group had a primary composite renal endpoint event (hazard ratio [HR]0·65 [95% CI 0·49–0·88]; p=0·0047). Fluid retention and anaemia adverse events, which have been previously attributed to endothelin receptor antagonists, were more frequent in the atrasentan group than in the placebo group. Hospital admission for heart failure occurred in 47 (3·5%)of 1325 patients in the atrasentan group and 34 (2·6%)of 1323 patients in the placebo group (HR 1·33 [95% CI 0·85–2·07]; p=0·208). 58 (4·4%)patients in the atrasentan group and 52 (3·9%)in the placebo group died (HR 1·09 [95% CI 0·75–1·59]; p=0·65). Interpretation: Atrasentan reduced the risk of renal events in patients with diabetes and chronic kidney disease who were selected to optimise efficacy and safety. These data support a potential role for selective endothelin receptor antagonists in protecting renal function in patients with type 2 diabetes at high risk of developing end-stage kidney disease. Funding: AbbVie

Genetic and structural validation of <em>Aspergillus fumigatus N</em>-acetylphosphoglucosamine mutase as an antifungal target

Aspergillus fumigatus is the causative agent of IA (invasive aspergillosis) in immunocompromised patients. It possesses a cell wall composed of chitin, glucan and galactomannan, polymeric carbohydrates synthesized by processive glycosyltransferases from intracellular sugar nucleotide donors. Here we demonstrate that A. fumigatus possesses an active AfAGM1 (A. fumigatus N-acetylphosphoglucosamine mutase), a key enzyme in the biosynthesis of UDP (uridine diphosphate)&#x2013;GlcNAc (N-acetylglucosamine), the nucleotide sugar donor for chitin synthesis. A conditional agm1 mutant revealed the gene to be essential. Reduced expression of agm1 resulted in retarded cell growth and altered cell wall ultrastructure and composition. The crystal structure of AfAGM1 revealed an amino acid change in the active site compared with the human enzyme, which could be exploitable in the design of selective inhibitors. AfAGM1 inhibitors were discovered by high-throughput screening, inhibiting the enzyme with IC50s in the low &#x03BC;M range. Together, these data provide a platform for the future development of AfAGM1 inhibitors with antifungal activity

Genome-wide scan for commons SNPs affecting bovine leukemia virus infection level in dairy cattle

Abstract Background Bovine leukemia virus (BLV) infection is omnipresent in dairy herds causing direct economic losses due to trade restrictions and lymphosarcoma-related deaths. Milk production drops and increase in the culling rate are also relevant and usually neglected. The BLV provirus persists throughout a lifetime and an inter-individual variation is observed in the level of infection (LI) in vivo. High LI is strongly correlated with disease progression and BLV transmission among herd mates. In a context of high prevalence, classical control strategies are economically prohibitive. Alternatively, host genomics studies aiming to dissect loci associated with LI are potentially useful tools for genetic selection programs tending to abrogate the viral spreading. The LI was measured through the proviral load (PVL) set–point and white blood cells (WBC) counts. The goals of this work were to gain insight into the contribution of SNPs (bovine 50KSNP panel) on LI variability and to identify genomics regions underlying this trait. Results We quantified anti–p24 response and total leukocytes count in peripheral blood from 1800 cows and used these to select 800 individuals with extreme phenotypes in WBCs and PVL. Two case-control genomic association studies using linear mixed models (LMMs) considering population stratification were performed. The proportion of the variance captured by all QC-passed SNPs represented 0.63 (SE ± 0.14) of the phenotypic variance for PVL and 0.56 (SE ± 0.15) for WBCs. Overall, significant associations (Bonferroni’s corrected -log10p > 5.94) were shared for both phenotypes by 24 SNPs within the Bovine MHC. Founder haplotypes were used to measure the linkage disequilibrium (LD) extent (r2 = 0.22 ± 0.27 at inter-SNP distance of 25−50 kb). The SNPs and LD blocks indicated genes potentially associated with LI in infected cows: i.e. relevant immune response related genes (DQA1, DRB3, BOLA-A, LTA, LTB, TNF, IER3, GRP111, CRISP1), several genes involved in cell cytoskeletal reorganization (CD2AP, PKHD1, FLOT1, TUBB5) and modelling of the extracellular matrix (TRAM2, TNXB). Host transcription factors (TFs) were also highlighted (TFAP2D; ABT1, GCM1, PRRC2A). Conclusions Data obtained represent a step forward to understand the biology of BLV–bovine interaction, and provide genetic information potentially applicable to selective breeding programs

Equalization of four cardiovascular risk algorithms after systematic recalibration: individual-participant meta-analysis of 86 prospective studies.

AIMS: There is debate about the optimum algorithm for cardiovascular disease (CVD) risk estimation. We conducted head-to-head comparisons of four algorithms recommended by primary prevention guidelines, before and after 'recalibration', a method that adapts risk algorithms to take account of differences in the risk characteristics of the populations being studied. METHODS AND RESULTS: Using individual-participant data on 360 737 participants without CVD at baseline in 86 prospective studies from 22 countries, we compared the Framingham risk score (FRS), Systematic COronary Risk Evaluation (SCORE), pooled cohort equations (PCE), and Reynolds risk score (RRS). We calculated measures of risk discrimination and calibration, and modelled clinical implications of initiating statin therapy in people judged to be at 'high' 10 year CVD risk. Original risk algorithms were recalibrated using the risk factor profile and CVD incidence of target populations. The four algorithms had similar risk discrimination. Before recalibration, FRS, SCORE, and PCE over-predicted CVD risk on average by 10%, 52%, and 41%, respectively, whereas RRS under-predicted by 10%. Original versions of algorithms classified 29-39% of individuals aged ≥40 years as high risk. By contrast, recalibration reduced this proportion to 22-24% for every algorithm. We estimated that to prevent one CVD event, it would be necessary to initiate statin therapy in 44-51 such individuals using original algorithms, in contrast to 37-39 individuals with recalibrated algorithms. CONCLUSION: Before recalibration, the clinical performance of four widely used CVD risk algorithms varied substantially. By contrast, simple recalibration nearly equalized their performance and improved modelled targeting of preventive action to clinical need