Medication-Assisted Treatment in the Hudson Headwaters Health Network

Background: Opioid use results in over 45,000 overdose deaths annually in the US, with rural areas disproportionately affected. While medication-assisted treatment (MAT) for opioid use disorder (OUD) is an effective intervention available through outpatient primary care, less than 25% of patients with OUD are currently in treatment. This study explored factors associated with patient retention in an MAT program offered by Hudson Headwaters, a Federally Qualified Health Center that serves a vast and mostly rural region of Northeastern New York. Methods: We included a total of 354 patients diagnosed with OUD who had at least two appointments for MAT between December 2016 and November 2019 in this analysis. We ran univariate and multivariate regression analyses to examine factors associated with overall retention. Results: The median age at the first MAT visit was 35.2 years (IQR=12.0), and 50% of patients self-identified as female. Overall, the one-year retention rate was 74.7% (95%CI=68.6-81.4). Increased risk for lower retention was seen among men (HR=1.7, 95%CI=1.0-2.8) and those not commercially insured (HR=3.2, 95%CI=1.1-8.7). Receiving MAT directly from a primary care provider greatly reduced the risk of lower retention (HR=0.4 ,95% CI=0.2-1.0). Roundtrip, median travel time to access care was 27.2 minutes (IQR=33.1). Although 12% of patients drove over 60 minutes to get to their MAT clinic, travel time and distance was not associated with retention. Conclusions: While some surveys have suggested that patient access to MAT clinics is a significant barrier to treatment, for this chiefly rural population, ease of access as measured by travel time and distance was less influential on outcomes than other patient- and provider-level factors. Potential recommendations to improve retention include engaging primary care providers in MAT provision and the use of case management services to address other socioeconomic barriers to treatment.https://scholarworks.uvm.edu/fmclerk/1626/thumbnail.jp

Determination of Soluble CD14 Molecular Weight Variants in Human Plasma

Inflammation is an important underlying biochemical process of many fatal diseases and infections. Inflammation can be an acute response to trauma or infection, or chronic in cardiovascular diseases like atherosclerosis. In the United States, in 2011 atherosclerosis was responsible for 16% of all deaths, and in 2015 an estimated 200,000 people will die from sepsis [1, 2]. The Cardiovascular Health Study (CHS) found that elevated plasma concentration of the inflammatory protein soluble CD14 (sCD14) independently predicts mortality from atherosclerotic cardiovascular diseases in older adults [3]. Genomewide SNPs explained approximately 33% of the sCD14 phenotypic variance. In European Americans, the strongest genome-wide association signal was centered around the CD14 structural gene [3], yet little is known about how these SNPs affect the circulating plasma sCD14 that was measured by ELISA in this study. We therefore sought to determine if different forms of sCD14, as measured by the ELISA in the CHS, could be detected in a small (N=15), presumably healthy human population. Utilizing gel filtration column chromatography to estimate molecular weights (MWs), sCD14 was detectable over a spectrum of MWs from 20kDa to 150kDa, and had an approximate peak around 55kDa. These data support previous research suggesting that there are multiple forms of sCD14 in human plasma. It appears that the ELISA is not detecting sCD14 on microparticle or a 13kDa fragment (sCD14-ST). There does appear to be a higher MW sCD14 form that seems to be primarily detectable between 71kDa to 87kD. A sCD14 form in this MW range has never been described in the literature. In order to describe the different sCD14 MW variants, further inquiry is needed into the precise MWs of each form of sCD14 in plasma

The Effect of Food Insecurity Training on Knowledge, Awareness, Screening, and Intervention Practices within Two Pediatric Wards at an Academic Medical Center

Background and Introduction • Food insecurity is a major driver of preventable disease. Providers can screen to identify patients at risk for food insecurity using a two-question survey tool called “The Hunger Vital Sign”. Screening barriers identified in the literature include lack of provider knowledge, comfort, and capacity for effective intervention. Addressing this provider knowledge gap through training is essential for implementing robust and sustainable clinical food insecurity screening practices. • This study aims to evaluate the effect of food insecurity education on providers’ knowledge and awareness of food insecurity and their likelihood to screen and make referrals for at-risk patients, as well as to encourage healthcare providers to foster a culture of food insecurity screening and intervention in their practices. Objectives 1. To determine providers’ knowledge of food insecurity and awareness of referral practices and resources to help patients experiencing food insecurity. 2. To determine if providers’ participation in formal food insecurity training influences their likelihood of incorporating food insecurity screening into their patient interviews. 3. To determine if providers’ action following a positive screen is affected by participating in food insecurity training.https://scholarworks.uvm.edu/comphp_gallery/1285/thumbnail.jp

Junior Recital

List of performers and performances

Dengue Virus Inhibits Immune Responses in Aedes aegypti Cells

The ability of many viruses to manipulate the host antiviral immune response often results in complex host-pathogen interactions. In order to study the interaction of dengue virus (DENV) with the Aedes aegypti immune response, we have characterized the DENV infection-responsive transcriptome of the immune-competent A. aegypti cell line Aag2. As in mosquitoes, DENV infection transcriptionally activated the cell line Toll pathway and a variety of cellular physiological systems. Most notably, however, DENV infection down-regulated the expression levels of numerous immune signaling molecules and antimicrobial peptides (AMPs). Functional assays showed that transcriptional induction of AMPs from the Toll and IMD pathways in response to bacterial challenge is impaired in DENV-infected cells. In addition, Escherichia coli, a Gram-negative bacteria species, grew better when co-cultured with DENV-infected cells than with uninfected cells, suggesting a decreased production of AMPs from the IMD pathway in virus-infected cells. Pre-stimulation of the cell line with Gram-positive bacteria prior to DENV infection had no effect on DENV titers, while pre-stimulation with Gram-negative bacteria resulted in an increase in DENV titers. These results indicate that DENV is capable of actively suppressing immune responses in the cells it infects, a phenomenon that may have important consequences for virus transmission and insect physiology

The James Webb Space Telescope Mission

Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least $4m$. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the $6.5m$ James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure

Inhibition of TGF-β and NOTCH Signaling by Cutaneous Papillomaviruses

Infections with cutaneous papillomaviruses have been linked to cutaneous squamous cell carcinomas that arise in patients who suffer from a rare genetic disorder, epidermodysplasia verruciformis, or those who have experienced long-term, systemic immunosuppression following organ transplantation. The E6 proteins of the prototypical cutaneous human papillomavirus (HPV) 5 and HPV8 inhibit TGF-β and NOTCH signaling. The Mus musculus papillomavirus 1, MmuPV1, infects laboratory mouse strains and causes cutaneous skin warts that can progress to squamous cell carcinomas. MmuPV1 E6 shares biological and biochemical activities with HPV8 E6 including the ability to inhibit TGF-β and NOTCH signaling by binding the SMAD2/SMAD3 and MAML1 transcription factors, respectively. Inhibition of TGF-β and NOTCH signaling is linked to delayed differentiation and sustained proliferation of differentiating keratinocytes. Furthermore, the ability of MmuPV1 E6 to bind MAML1 is necessary for wart and cancer formation in experimentally infected mice. Hence, experimental MmuPV1 infection in mice will be a robust and valuable experimental system to dissect key aspects of cutaneous HPV infection, pathogenesis, and carcinogenesis