Interview with Joy Slayton

Ms. Slayton shares about her life growing up in Arkansas and raising kids here at Harding

Efficacy of a nootropic spearmint extract on reactive agility: a randomized, double-blind, placebo-controlled, parallel trial

Abstract Background Proprietary spearmint extract (PSE) containing a minimum 14.5% rosmarinic acid and 24% total phenolic content, has evinced positive effects on cognition in individuals aged 50–70 with memory impairment after chronic supplementation. To address the growing interest in connecting mental and physical performance, the present study examined whether the nootropic effects of PSE translate into changes in reactive agility following daily supplementation with PSE. Methods Utilizing a randomized, double-blind, placebo-controlled, parallel design, healthy, recreationally-active men and women (n = 142) received 900 mg of PSE or placebo (PLA) daily for 90 days. Reactive agility, our primary outcome, was determined by measuring the number of hits and average reaction time (ART) on a Makoto Arena II, a 3600 audio-visual device that measures stationary, lateral, and multi-directional active choice reaction performance. Safety was evaluated using complete blood count, comprehensive metabolic panel, and blood lipids. Measurements were evaluated on days 7, 30, and 90 of supplementation. Results An overall treatment effect (p = 0.019) was evident for increased hits with PSE on the stationary test with footplates, with between group differences at Day 30 (PSE vs. PLA: 28.96 ± 2.08 vs. 28.09 ± 1.92 hits; p = 0.040) and Day 90 (PSE vs. PLA: 28.42 ± 2.54 vs. 27.02 ± 3.55 hits; p = 0.002). On the same task, ART improved (treatment effect, p = 0.036) with PSE at Day 7 (PSE vs. PLA: 0.5896 ± 0.060 vs. 0.6141 ± 0.073 s; p = 0.049) and Day 30 (PSE vs. PLA: 0.5811 ± 0.068 vs. 0.6033 ± 0.055 s; p = 0.049). PSE also significantly increased hits (treatment effect, p = 0.020) at Day 30 (PSE vs. PLA: 19.25 ± 1.84 vs. 18.45 ± 1.48 hits; p = 0.007) and Day 90 (PSE vs. PLA: 19.39 ± 1.90 vs. 18.66 ± 1.64 hits; p = 0.026) for the multi-directional test with footplates. Significant differences were not observed in the remaining Makoto tests. PSE was well tolerated as evidenced by no effects observed in the blood safety panels. Conclusions The findings of the current study demonstrate that consumption of 900 mg of PSE improved specific measures of reactive agility in a young, active population. Trial registration clinicaltrials.gov, NCT02518165. Registered August 7, 2015 – retrospectively registered

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease