Factors Influencing Pediatric Dental Program Directorsâ Selection of Residents and Demographics of Current Directors

The primary goal of this study was to examine the criteria that influence rankings of candidates by advanced education program directors in pediatric dentistry. Secondary objectives were to obtain information on the resident selection process and to explore demographics of current program directors. A survey was sent in 2005 to all sixtyâ three program directors of pediatric dentistry residency programs accredited within the United States for the graduating class of 2007. The survey had a response rate of almost 78 percent (49/63). Respondents were requested to rank the importance of eleven factors that are typically included in the selection criteria for pediatric dentistry residents. Factors were rated on a scale of critical, very important, fairly important, somewhat important, and not important. The four highest ranked criteria by program directors were the following, in order: National Board scores, dental school clinical grades, class rank, and grade point average (GPA). Other factors ranked in descending order of perceived importance were the following: dental school basic science grades, experience in pediatric dentistry, extracurricular activities, completion of a general practice residency or advanced education in general dentistry program, the application essay, a publication or professional presentation, and private practice experience. All directors ranked personal interviews as very important to critical. Letters of recommendation from a pediatric dentistry department chairperson or faculty member were viewed more favorably than letters from dental school deans and nonâ pediatric dentistry faculty. Fiftyâ seven percent of the directors responding (28/49) were male, and 81 percent (40/49) were white, nonâ Hispanic. Fiftyâ nine percent of the directors (29/49) graduated from a residency program over twenty years ago, with 39 percent (19/49) having been a director for less than five years.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/153594/1/jddj002203372009733tb04706x.pd

CASTAway : An asteroid main belt tour and survey

CASTAway is a mission concept to explore our Solar System's main asteroid belt. Asteroids and comets provide a window into the formation and evolution of our Solar System and the composition of these objects can be inferred from space-based remote sensing using spectroscopic techniques. Variations in composition across the asteroid populations provide a tracer for the dynamical evolution of the Solar System. The mission combines a long-range (point source) telescopic survey of over 10,000 objects, targeted close encounters with 10-20 asteroids and serendipitous searches to constrain the distribution of smaller (e.g. 10 m) size objects into a single concept. With a carefully targeted trajectory that loops through the asteroid belt, CASTAway would provide a comprehensive survey of the main belt at multiple scales. The scientific payload comprises a 50 cm diameter telescope that includes an integrated low-resolution (R = 30-100) spectrometer and visible context imager, a thermal (e.g. 6-16 mu m) imager for use during the flybys, and modified star tracker cameras to detect small (similar to 10 m) asteroids. The CASTAway spacecraft and payload have high levels of technology readiness and are designed to fit within the programmatic and cost caps for a European Space Agency medium class mission, while delivering a significant increase in knowledge of our Solar System. (C) 2017 COSPAR. Published by Elsevier Ltd. All rights reserved.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 hospitalization2–4 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

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