A Geology Sampling System for Small Bodies

Human exploration of microgravity bodies is being investigated as a precursor to a Mars surface mission. Asteroids, comets, dwarf planets, and the moons of Mars all fall into this microgravity category and some are being discussed as potential mission targets. Obtaining geological samples for return to Earth will be a major objective for any mission to a small body. Currently, the knowledge base for geology sampling in microgravity is in its infancy. Humans interacting with non-engineered surfaces in microgravity environment pose unique challenges. In preparation for such missions a team at the NASA Johnson Space Center has been working to gain experience on how to safely obtain numerous sample types in such an environment. This paper describes the type of samples the science community is interested in, highlights notable prototype work, and discusses an integrated geology sampling solution

Association Between Medication Adherence and the Outcomes of Heart Failure

Background Previous studies of heart failure patients have demonstrated an association between cardiovascular medication adherence and hospitalizations or a composite end point of hospitalization and death. Few studies have assessed the impact of treatment adherence within large general medical populations that distinguish the health outcomes of emergency department visits, hospitalization, and death. Objective To determine the association of incremental cardiovascular medication adherence on emergency department visits, hospitalization, and death in adult heart failure patients in Indiana. Design Retrospective cohort study conducted using electronic health record data from the statewide Indiana Network for Patient Care (INPC) between 2004 and 2009. Methods Patients were at least 18 years of age with a diagnosis of heart failure and prescribed at least one cardiovascular medication for heart failure. Adherence was measured as the proportion of days covered (PDC) using pharmacy transaction data. Clinical end points included emergency department visits, hospital admissions, length of hospital stay, and mortality. Generalized linear models were used to determine the effect of a 10% increase in PDC on clinical end points adjusting for age, sex, race, Charlson comorbidity index, and medications. Results Electronic health records were available for 55,312 patients (mean age ± standard deviation [SD] 68 ± 16 years; 54% women; 65% white). Mean PDC for all heart failure medications was 63% ± 23%. For every 10% increase in PDC, emergency department visits decreased 11% (rate ratio [RR] 0.89; 95% confidence interval [CI] 0.89‐0.89), hospital admissions decreased 6% (RR 0.94; 95% CI 0.94‐0.94), total length of hospital stay decreased 1% (RR 0.99; 95% CI 0.99‐1.00), and all‐cause mortality decreased 9% (odds ratio 0.91; 95% CI 0.90‐0.92). Conclusion Incremental medication adherence was associated with reductions in emergency department visits, hospital admissions, length of hospital stay, and all‐cause mortality

The Vehicle, 1967, Vol. 9 no. 1

Vol. 9, No. 1 Table of Contents Commentarypage 3 PoofMolly J. Evanspage 4 PreludeMike Baldwinpage 5 UntitledMike Baldwinpage 5 Where is Tomorrow?Paula Bresnanpage 6 Could It Be Or NotMary Hoeggerpage 7 PsalmAnthony Griggspage 7 Where Am I Going?William A. Framepage 8 Out of DarknessMarilyn Henry Hoodpage 9 She CriedMolly J. Evanspage 12 When I MoveAnthony Griggspage 13 Hi Ya, MorningWilliam A. Framepage 13 Summer Twilight ThoughtsSteve Allenpage 14 Too MuchBill Moserpage 16 Ink SketchWilliam A. Framepage 17 No. 1Molly J. Evanspage 18 Youth, So Hated and DamnedJeff Hendrickspage 18 GoneJackie Jaquespage 19 The JesterWilliam A. Framepage 20 ReflectionMike Baldwinpage 20 No. 3Molly J. Evanspage 21 EpitaphBill Moserpage 22 I Take A Long-Out-of-Use BookAnthony Griggspage 23https://thekeep.eiu.edu/vehicle/1016/thumbnail.jp

The Vehicle, 1967, Vol. 9 no. 1

Vol. 9, No. 1 Table of Contents Commentarypage 3 PoofMolly J. Evanspage 4 PreludeMike Baldwinpage 5 UntitledMike Baldwinpage 5 Where is Tomorrow?Paula Bresnanpage 6 Could It Be Or NotMary Hoeggerpage 7 PsalmAnthony Griggspage 7 Where Am I Going?William A. Framepage 8 Out of DarknessMarilyn Henry Hoodpage 9 She CriedMolly J. Evanspage 12 When I MoveAnthony Griggspage 13 Hi Ya, MorningWilliam A. Framepage 13 Summer Twilight ThoughtsSteve Allenpage 14 Too MuchBill Moserpage 16 Ink SketchWilliam A. Framepage 17 No. 1Molly J. Evanspage 18 Youth, So Hated and DamnedJeff Hendrickspage 18 GoneJackie Jaquespage 19 The JesterWilliam A. Framepage 20 ReflectionMike Baldwinpage 20 No. 3Molly J. Evanspage 21 EpitaphBill Moserpage 22 I Take A Long-Out-of-Use BookAnthony Griggspage 23https://thekeep.eiu.edu/vehicle/1016/thumbnail.jp

Utility of pharmacogenetic testing to optimise antidepressant pharmacotherapy in youth: a narrative literature review

Pharmacogenetics (PGx) is the study and application of how interindividual differences in our genomes can influence drug responses. By evaluating individuals’ genetic variability in genes related to drug metabolism, PGx testing has the capabilities to individualise primary care and build a safer drug prescription model than the current “one-size-fits-all” approach. In particular, the use of PGx testing in psychiatry has shown promising evidence in improving drug efficacy as well as reducing toxicity and adverse drug reactions. Despite randomised controlled trials demonstrating an evidence base for its use, there are still numerous barriers impeding its implementation. This review paper will discuss the management of mental health conditions with PGx-guided treatment with a strong focus on youth mental illness. PGx testing in clinical practice, the concerns for its implementation in youth psychiatry, and some of the barriers inhibiting its integration in clinical healthcare will also be discussed. Overall, this paper provides a comprehensive review of the current state of knowledge and application for PGx in psychiatry and summarises the capabilities of genetic information to personalising medicine for the treatment of mental ill-health in youth

Teratology Primer-2nd Edition (7/9/2010)

Foreword: What is Teratology? “What a piece of work is an embryo!” as Hamlet might have said. “In form and moving how express and admirable! In complexity how infinite!” It starts as a single cell, which by repeated divisions gives rise to many genetically identical cells. These cells receive signals from their surroundings and from one another as to where they are in this ball of cells —front or back, right or left, headwards or tailwards, and what they are destined to become. Each cell commits itself to being one of many types; the cells migrate, combine into tissues, or get out of the way by dying at predetermined times and places. The tissues signal one another to take their own pathways; they bend, twist, and form organs. An organism emerges. This wondrous transformation from single celled simplicity to myriad-celled complexity is programmed by genes that, in the greatest mystery of all, are turned on and off at specified times and places to coordinate the process. It is a wonder that this marvelously emergent operation, where there are so many opportunities for mistakes, ever produces a well-formed and functional organism. And sometimes it doesn’t. Mistakes occur. Defective genes may disturb development in ways that lead to death or to malformations. Extrinsic factors may do the same. “Teratogenic” refers to factors that cause malformations, whether they be genes or environmental agents. The word comes from the Greek “teras,” for “monster,” a term applied in ancient times to babies with severe malformations, which were considered portents or, in the Latin, “monstra.” Malformations can happen in many ways. For example, when the neural plate rolls up to form the neural tube, it may not close completely, resulting in a neural tube defect—anencephaly if the opening is in the head region, or spina bifida if it is lower down. The embryonic processes that form the face may fail to fuse, resulting in a cleft lip. Later, the shelves that will form the palate may fail to move from the vertical to the horizontal, where they should meet in the midline and fuse, resulting in a cleft palate. Or they may meet, but fail to fuse, with the same result. The forebrain may fail to induce the overlying tissue to form the eye, so there is no eye (anophthalmia). The tissues between the toes may fail to break down as they should, and the toes remain webbed. Experimental teratology flourished in the 19th century, and embryologists knew well that the development of bird and frog embryos could be deranged by environmental “insults,” such as lack of oxygen (hypoxia). But the mammalian uterus was thought to be an impregnable barrier that would protect the embryo from such threats. By exclusion, mammalian malformations must be genetic, it was thought. In the early 1940s, several events changed this view. In Australia an astute ophthalmologist, Norman Gregg, established a connection between maternal rubella (German measles) and the triad of cataracts, heart malformations, and deafness. In Cincinnati Josef Warkany, an Austrian pediatrician showed that depriving female rats of vitamin B (riboflavin) could cause malformations in their offspring— one of the early experimental demonstrations of a teratogen. Warkany was trying to produce congenital cretinism by putting the rats on an iodine deficient diet. The diet did indeed cause malformations, but not because of the iodine deficiency; depleting the diet of iodine had also depleted it of riboflavin! Several other teratogens were found in experimental animals, including nitrogen mustard (an anti cancer drug), trypan blue (a dye), and hypoxia (lack of oxygen). The pendulum was swinging back; it seemed that malformations were not genetically, but environmentally caused. In Montreal, in the early 1950s, Clarke Fraser’s group wanted to bring genetics back into the picture. They had found that treating pregnant mice with cortisone caused cleft palate in the offspring, and showed that the frequency was high in some strains and low in others. The only difference was in the genes. So began “teratogenetics,” the study of how genes influence the embryo’s susceptibility to teratogens. The McGill group went on to develop the idea that an embryo’s genetically determined, normal, pattern of development could influence its susceptibility to a teratogen— the multifactorial threshold concept. For instance, an embryo must move its palate shelves from vertical to horizontal before a certain critical point or they will not meet and fuse. A teratogen that causes cleft palate by delaying shelf movement beyond this point is more likely to do so in an embryo whose genes normally move its shelves late. As studies of the basis for abnormal development progressed, patterns began to appear, and the principles of teratology were developed. These stated, in summary, that the probability of a malformation being produced by a teratogen depends on the dose of the agent, the stage at which the embryo is exposed, and the genotype of the embryo and mother. The number of mammalian teratogens grew, and those who worked with them began to meet from time to time, to talk about what they were finding, leading, in 1960, to the formation of the Teratology Society. There were, of course, concerns about whether these experimental teratogens would be a threat to human embryos, but it was thought, by me at least, that they were all “sledgehammer blows,” that would be teratogenic in people only at doses far above those to which human embryos would be exposed. So not to worry, or so we thought. Then came thalidomide, a totally unexpected catastrophe. The discovery that ordinary doses of this supposedly “harmless” sleeping pill and anti-nauseant could cause severe malformations in human babies galvanized this new field of teratology. Scientists who had been quietly working in their laboratories suddenly found themselves spending much of their time in conferences and workshops, sitting on advisory committees, acting as consultants for pharmaceutical companies, regulatory agencies, and lawyers, as well as redesigning their research plans. The field of teratology and developmental toxicology expanded rapidly. The following pages will show how far we have come, and how many important questions still remain to be answered. A lot of effort has gone into developing ways to predict how much of a hazard a particular experimental teratogen would be to the human embryo (chapters 9–19). It was recognized that animal studies might not prove a drug was “safe” for the human embryo (in spite of great pressure from legislators and the public to do so), since species can vary in their responses to teratogenic exposures. A number of human teratogens have been identified, and some, suspected of teratogenicity, have been exonerated—at least of a detectable risk (chapters 21–32). Regulations for testing drugs before market release have greatly improved (chapter 14). Other chapters deal with how much such things as population studies (chapter 11), post-marketing surveillance (chapter 13), and systems biology (chapter 16) add to our understanding. And, in a major advance, the maternal role of folate in preventing neural tube defects and other birth defects is being exploited (chapter 32). Encouraging women to take folic acid supplements and adding folate to flour have produced dramatic falls in the frequency of neural tube defects in many parts of the world. Progress has been made not only in the use of animal studies to predict human risks, but also to illumine how, and under what circumstances, teratogens act to produce malformations (chapters 2–8). These studies have contributed greatly to our knowledge of abnormal and also normal development. Now we are beginning to see exactly when and where the genes turn on and off in the embryo, to appreciate how they guide development and to gain exciting new insights into how genes and teratogens interact. The prospects for progress in the war on birth defects were never brighter. F. Clarke Fraser McGill University (Emeritus) Montreal, Quebec, Canad

Is Inequality Among Universities Increasing? Gini Coefficients and the Elusive Rise of Elite Universities

One of the unintended consequences of the New Public Management (NPM) in universities is often feared to be a division between elite institutions focused on research and large institutions with teaching missions. However, institutional isomorphisms provide counter-incentives. For example, university rankings focus on certain output parameters such as publications, but not on others (e.g., patents). In this study, we apply Gini coefficients to university rankings in order to assess whether universities are becoming more unequal, at the level of both the world and individual nations. Our results do not support the thesis that universities are becoming more unequal. If anything, we predominantly find homogenization, both at the level of the global comparisons and nationally. In a more restricted dataset (using only publications in the natural and life sciences), we find increasing inequality for those countries, which used NPM during the 1990s, but not during the 2000s. Our findings suggest that increased output steering from the policy side leads to a global conformation to performance standards

Cognitive and environmental predictors of early literacy skills

Not all young children benefit from book exposure in preschool age. It is claimed that the ability to hold information in mind (short-term memory), to ignore distraction (inhibition), and to focus attention and stay focused (sustained attention) may have a moderating effect on children’s reactions to the home literacy environment. In a group of 228 junior kindergarten children with a native Dutch background, with a mean age of 54.29 months (SD = 2.12 months), we explored therefore the relationship between book exposure, cognitive control and early literacy skills. Parents filled in a HLE questionnaire (book sharing frequency and an author recognition checklist as indicator of parental leisure reading habits), and children completed several tests in individual sessions with the researcher (a book-cover recognition test, PPVT, letter knowledge test, the subtests categories and patterns of the SON, and cognitive control measures namely digit span of the KABC, a peg tapping task and sustained attention of the ANT). Main findings were: (1) Children’s storybook knowledge mediated the relationship between home literacy environment and literacy skills. (2) Both vocabulary and letter knowledge were predicted by book exposure. (3) Short-term memory predicted vocabulary over and above book exposure. (4) None of the cognitive control mechanisms moderated the beneficial effects of book exposure

The JWST Early Release Science Program for Direct Observations of Exoplanetary Systems II: A 1 to 20 Micron Spectrum of the Planetary-Mass Companion VHS 1256-1257 b

We present the highest fidelity spectrum to date of a planetary-mass object. VHS 1256 b is a $<$20 M$_\mathrm{Jup}$ widely separated ($\sim$8\arcsec, a = 150 au), young, planetary-mass companion that shares photometric colors and spectroscopic features with the directly imaged exoplanets HR 8799 c, d, and e. As an L-to-T transition object, VHS 1256 b exists along the region of the color-magnitude diagram where substellar atmospheres transition from cloudy to clear. We observed VHS 1256~b with \textit{JWST}'s NIRSpec IFU and MIRI MRS modes for coverage from 1 $\mu$m to 20 $\mu$m at resolutions of $\sim$1,000 - 3,700. Water, methane, carbon monoxide, carbon dioxide, sodium, and potassium are observed in several portions of the \textit{JWST} spectrum based on comparisons from template brown dwarf spectra, molecular opacities, and atmospheric models. The spectral shape of VHS 1256 b is influenced by disequilibrium chemistry and clouds. We directly detect silicate clouds, the first such detection reported for a planetary-mass companion.Comment: Accepted ApJL Iterations of spectra reduced by the ERS team are hosted at this link: https://github.com/bemiles/JWST_VHS1256b_Reduction/tree/main/reduced_spectr