The Level of Europium-154 Contaminating Samarium-153-EDTMP Activates the Radiation Alarm System at the US Homeland Security Checkpoints

153Sm-EDTMP is a radiopharmaceutical composed of EDTMP (ethylenediamine-tetramethylenephosphonate) and Samarium-153 [1]. 153Sm-EDTMP has an affinity for skeletal tissue and concentrates in areas with increased bone turnover; thus, it is successfully used in relieving pain related to diffuse bone metastases [1]. The manufacturing process of 153Sm-EDTMP leads to contamination with 154Eu (Europium-154) [2]. A previous study only alluded to the retention of 154Eu in the bones after receiving treatment with 153Sm-EDTMP [2]. Activation of the alarm at security checkpoints after 153Sm-EDTMP therapy has not been previously reported. Two out of 15 patients who received 153Sm-EDTMP at Roger Maris Cancer Center (Fargo, N. Dak., USA) activated the radiation activity sensors while passing through checkpoints; one at a US airport and the other while crossing the American-Canadian border. We assume that the 154Eu which remained in the patients’ bones activated the sensors

The Grizzly, February 9, 1990

Students Grapple With Rising Costs • USEAC Plants Seeds for First Ursinus Earth Day • Letter: Cynosure Cynic • Michener Bids Campus Adieu • The Trojans are Coming • Get your Act in Gear • Feb 14: A Woman\u27s Holiday? • UC Aquabears Squash Susquehanna • Susquehanna Drowned • Hoopsters Split Again • Making Tracks • Wismer Looking Gamely • Stop The Sex Wars • Grapplers Rebound With Big Victory • Gymnasts Prepare for Nationals • Athletes of the Week • Countdownhttps://digitalcommons.ursinus.edu/grizzlynews/1251/thumbnail.jp

The Grizzly, January 26, 1990

Campus Additions are Muddling Thru • Dennis Gould Makes His Life in Art With Inner Voice • Letters: GDI Supports Power\u27s Points; Corson Operator Boxing Impersonal; Fashion Focus Offensive • A Civil Voice Inspires • Bookstore Buyback Prices Fair? • UC Hoopsters Have Winning Potential! • Slippery When Wet! • Aquabears: Quality not Quantity • Lady Tumblers Hopeful • Grappling to Victory • Corson Special: Phone in a Box • Student Symposium • Lantern Finally Here • Vacancies Filled • Bears On Their Way! • Athletes of the Week • Changes on Track • Student-Faculty Interactions Beneficial for Both • Kriebel to Lecture at Museum • Workshops Offeredhttps://digitalcommons.ursinus.edu/grizzlynews/1249/thumbnail.jp

The Grizzly, February 26, 1990

UC Airband Gets Respect It Deserves • Student Abortion Debate To Heat Campus • Letters: Hey, Don\u27t be so Rude; Pledging: A Test; Don\u27t Blame Townies • Olin Topped In Style • New Day For Grizzly • Bears End Season With a Win • Bear Pack Paces To Second • Smith\u27s Super Season • Men Finish Sixth Aquabears Make a Splash • Grapplers To MAC\u27s • Haircuts Work Well • Richter Rips Alum • Trees Vanish In Northwest • Skateboarders Unite! • Rising Standards For Prospective Ursinus Students • Speaker Chosen • Martial Law Declared: Identification Now! • Hey Congress: Pass It, Man! • The King Of History • Bomberger Concert a Hit • Randolph Promoted • Bush Bugs Druggieshttps://digitalcommons.ursinus.edu/grizzlynews/1253/thumbnail.jp

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 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

A first update on mapping the human genetic architecture of COVID-19

peer reviewe

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 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

Mineral Composition of Beef Cattle Carcasses

Mineral retention was measured in 76 beef steers. Cattle were grown at different rates of gain and then finished on a common diet. Calcium and P retention were not affected by treatment and were similar between the growing and finishing periods averaging 4.2 g P and 10.8 g Ca /100 g protein gain across both experiments. As ADG during the growing period was decreased, K, Mg, and S mineral retention during the finishing period were increased. Expressing mineral retention as g/100 g protein gain reducedvariation due to animal size and ADG and suggests that current NRC predictions are accurate

Engineering Performance

Informatio