Michael Nixon

Over the last few weeks I have been delighted to get to know an individual who will become an integral part of the senior leadership team at Andrews University. His resume spoke to some of his life priorities and his accomplishments, and that was encouraging. But it is Michael Nixon as a person, his story, that I will share with the campus community today as I want you to meet the person I have met over the last few weeks: Caring, passionate, faithful, hopeful, determined and thoughtful. You will have much more of an opportunity to meet Michael as he takes up his position as Vice President for Diversity & Inclusion on August 1; however, in the meantime, here is a window into the story of our newest vice president. In 2009, Michael graduated from Andrews University. Up to that point, his life had been comparatively sheltered within the Seventh-day Adventist community, though he had enjoyed some diverse experiences during his college years, studying at Antillean University (Puerto Rico), Oakwood University (Alabama) and then Andrews. However, upon his graduation he decided to broaden his horizons and step out of his comfort zone. This journey took him as an AmeriCorps worker to a Catholic university, through law school, involved him with work for immigrant populations and ended with his role as a civil rights attorney in New York, specifically in the arena of fair housing. Those are the facts, but behind those facts is the story of an individual who has had to face challenging decisions on his faith commitment and his choice of priorities. In making his choices, Michael’s passion for his faith has deepened, and so has his understanding and commitment to equity and inclusion. In the last few years he has shown unequivocally that when it comes to faith and career, faith must come first. And when he has chosen where to walk it has been to walk alongside the disadvantaged, rather than where he might find visible personal success. Please do take the opportunity to get to know Michael better through his own words, as he shares his story through the lens of a critical moment in his life. Read his story in Stories of Andrews. Thank you, Michael, for taking the step to join us at Andrews University and share with us your skills, talents and passion for faith and diversity. You represent the spirit of Andrews and we welcome you to our—and your—campus! Andrea Luxtonhttps://digitalcommons.andrews.edu/stories-2017-summer/1000/thumbnail.jp

Effects of Naltrexone on Alcohol and Nicotine Use in Female P Rats

The objective of the present study was to determine the effectiveness of the opioid antagonist naltrexone at reducing the consumption of EtOH and nicotine in female alcohol-preferring (P) rats. P rats have been selectively bred to have a genetic predisposition for alcohol abuse, which allows them to be used as an animal model of alcoholism. P rats readily self-administer i.v nicotine (Le et al., 2016), have EtOH consumption during adolescence that is similar to that seen in adulthood, and operantly respond for EtOH until they are impaired/intoxicated (Bell et al., 2006). Thus, P rats are a useful model for studying naltrexone’s effects on EtOH and nicotine co-use

Lipid Profiles from Dried Blood Spots Reveal Lipidomic Signatures of Newborns Undergoing Mild Therapeutic Hypothermia after Hypoxic-Ischemic Encephalopathy.

Hypoxic-ischemic encephalopathy (HIE) is associated with perinatal brain injury, which may lead to disability or death. As the brain is a lipid-rich organ, various lipid species can be significantly impacted by HIE and these correlate with specific changes to the lipidomic profile in the circulation. Objective: To investigate the peripheral blood lipidomic signature in dried blood spots (DBS) from newborns with HIE. Using univariate analysis, multivariate analysis and sPLS-DA modelling, we show that newborns with moderate-severe HIE (n = 46) who underwent therapeutic hypothermia (TH) displayed a robust peripheral blood lipidomic signature comprising 29 lipid species in four lipid classes; namely phosphatidylcholine (PC), lysophosphatidylcholine (LPC), triglyceride (TG) and sphingomyelin (SM) when compared with newborns with mild HIE (n = 18). In sPLS-DA modelling, the three most discriminant lipid species were TG 50:3, TG 54:5, and PC 36:5. We report a reduction in plasma TG and SM and an increase in plasma PC and LPC species during the course of TH in newborns with moderate-severe HIE, compared to a single specimen from newborns with mild HIE. These findings may guide the research in nutrition-based intervention strategies after HIE in synergy with TH to enhance neuroprotection.NIHR Cambridge Biomedical Research Centre (146281) & Biotechnology and Biological Sciences Research Council (BB/P028195/1

An improved model of ethanol and nicotine co-use in female P rats: Effects of naltrexone, varenicline, and the selective nicotinic α6β2* antagonist r-bPiDI

Background Although pharmacotherapies are available for alcohol (EtOH) or tobacco use disorders individually, it may be possible to develop a single pharmacotherapy to treat heavy drinking tobacco smokers by capitalizing on the commonalities in their mechanisms of action. Methods Female alcohol-preferring (P) rats were trained for EtOH drinking and nicotine self-administration in two phases: (1) EtOH alone (0 vs. 15% EtOH, 2-bottle choice) and (2) concomitant access, during which EtOH access continued with access to nicotine (0.03 mg/kg/infusion, i.v.) using a 2-lever choice procedure (active vs. inactive lever) in which the fixed ratio (FR) requirement was gradually increased to FR30. When stable co-use was obtained, rats were pretreated with varying doses of naltrexone, varenicline, or r-bPiDI, an α6β2* subtype-selective nicotinic acetylcholine receptor antagonist shown previously to reduce nicotine self-administration. Results While EtOH intake was initially suppressed in phase 2 (co-use), pharmacologically relevant intake for both substances was achieved by raising the “price” of nicotine to FR30. In phase 2, naltrexone decreased EtOH and water consumption but not nicotine intake; in contrast, naltrexone in phase 1 (EtOH only) did not significantly alter EtOH intake. Varenicline and r-bPiDI in phase 2 both decreased nicotine self-administration and inactive lever pressing, but neither altered EtOH or water consumption. Conclusions These results indicate that increasing the “price” of nicotine increases EtOH intake during co-use. Additionally, the efficacy of naltrexone, varenicline, and r-bPiDI was specific to either EtOH or nicotine, with no efficacy for co-use. Nevertheless, future studies on combining these treatments may reveal synergistic efficacy

Results from the Atacama B-mode Search (ABS) Experiment

The Atacama B-mode Search (ABS) is an experiment designed to measure cosmic microwave background (CMB) polarization at large angular scales ($\ell>40$). It operated from the ACT site at 5190~m elevation in northern Chile at 145 GHz with a net sensitivity (NEQ) of 41 $\mu$K$\sqrt{\rm s}$. It employed an ambient-temperature sapphire half-wave plate rotating at 2.55 Hz to modulate the incident polarization signal and reduce systematic effects. We report here on the analysis of data from a 2400 deg$^2$ patch of sky centered at declination $-42^\circ$ and right ascension $25^\circ$. We perform a blind analysis. After unblinding, we find agreement with the Planck TE and EE measurements on the same region of sky. We marginally detect polarized dust emission and give an upper limit on the tensor-to-scalar ratio of $r<2.3$ (95% cl) with the equivalent of 100 on-sky days of observation. We also present a new measurement of the polarization of Tau A and introduce new methods associated with HWP-based observations.Comment: 38 pages, 11 figure

Antenatal corticosteroids and the renin-angiotensin-aldosterone system in adolescents born preterm

Antenatal corticosteroid (ANCS) treatment hastens fetal lung maturity and improves survival of premature infants, but the long-term effects of ANCS are not well-described. Animal models suggest ANCS increases the risk of cardiovascular disease through programmed changes in the renin-angiotensin (Ang)-aldosterone system (RAAS). We hypothesized that ANCS exposure alters the RAAS in adolescents born prematurely

Effects of the nicotinic agonist varenicline, nicotinic antagonist r-bPiDI, and DAT inhibitor R-modafinil on co-use of ethanol and nicotine in female P rats.

Rationale: Co-users of alcohol and nicotine are the largest group of polysubstance users worldwide. Commonalities in mechanisms of action for ethanol (EtOH) and nicotine proposes the possibility of developing a single pharmacotherapeutic to treat co-use. Objectives: Toward developing a preclinical model of co-use, female alcohol-preferring (P) rats were trained for voluntary EtOH drinking and i.v. nicotine self-administration in three phases: (1) EtOH alone (0 vs. 15%, 2-bottle choice); (2) nicotine alone (0.03 mg/kg/infusion, active vs. inactive lever); and (3) concurrent access to both EtOH and nicotine. Using this model, we examined the effects of (1) varenicline, a nicotinic acetylcholine receptor (nAChR) partial agonist with high affinity for the α4β2 subtype; (2) r-bPiDI, a subtype-selective antagonist at α6β2* nAChRs; and (3) (R)-modafinil, an atypical inhibitor of the dopamine transporter (DAT). Results: In Phases 1 and 2, pharmacologically relevant intake of EtOH and nicotine was achieved. In the concurrent access phase (Phase 3), EtOH consumption decreased while nicotine intake increased relative to Phases 1 and 2. For drug pretreatments, in the EtOH access phase (Phase 1), (R)-modafinil (100 mg/kg) decreased EtOH consumption, with no effect on water consumption. In the concurrent access phase, varenicline (3 mg/kg), r-bPiDI (20 mg/kg), and (R)-modafinil (100 mg/kg) decreased nicotine self-administration, but did not alter EtOH consumption, water consumption, or inactive lever pressing. Conclusions: These results indicate that therapeutics which may be useful for smoking cessation via selective inhibition of α4β2 or α6β2* nAChRs, or DAT inhibition, may not be sufficient to treat EtOH and nicotine co-use

Novel mutations expand the clinical spectrum of DYNC1H1-associated spinal muscular atrophy

OBJECTIVE To expand the clinical phenotype of autosomal dominant congenital spinal muscular atrophy with lower extremity predominance (SMA-LED) due to mutations in the dynein, cytoplasmic 1, heavy chain 1 (DYNC1H1) gene. METHODS Patients with a phenotype suggestive of a motor, non-length-dependent neuronopathy predominantly affecting the lower limbs were identified at participating neuromuscular centers and referred for targeted sequencing of DYNC1H1. RESULTS We report a cohort of 30 cases of SMA-LED from 16 families, carrying mutations in the tail and motor domains of DYNC1H1, including 10 novel mutations. These patients are characterized by congenital or childhood-onset lower limb wasting and weakness frequently associated with cognitive impairment. The clinical severity is variable, ranging from generalized arthrogryposis and inability to ambulate to exclusive and mild lower limb weakness. In many individuals with cognitive impairment (9/30 had cognitive impairment) who underwent brain MRI, there was an underlying structural malformation resulting in polymicrogyric appearance. The lower limb muscle MRI shows a distinctive pattern suggestive of denervation characterized by sparing and relative hypertrophy of the adductor longus and semitendinosus muscles at the thigh level, and diffuse involvement with relative sparing of the anterior-medial muscles at the calf level. Proximal muscle histopathology did not always show classic neurogenic features. CONCLUSION Our report expands the clinical spectrum of DYNC1H1-related SMA-LED to include generalized arthrogryposis. In addition, we report that the neurogenic peripheral pathology and the CNS neuronal migration defects are often associated, reinforcing the importance of DYNC1H1 in both central and peripheral neuronal functions