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Bryan Boyer

· Director of Bachelor of Science in Urban Technology, Associate Professor of Practice in Architecture

University of Michigan · Architecture

Active 2016–2022

h-index3
Citations61
Papers51 last 5y
Funding
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About

Bryan Boyer is cofounder of the architecture and strategic design studio Dash Marshall, where he runs the studio's strategic design practice working with clients such as Google, Sidewalk Labs, IKEA, Bloomberg Philanthropies, and the Museum of Modern Art to understand and envision how technology enables urban ways of life. He is also an Associate Professor of Practice in Architecture and the Director of the Bachelor of Science in Urban Technology degree at Taubman College of Architecture and Urban Planning at the University of Michigan. Boyer's professional background combines design, technology, and government innovation, and he has previously co-founded Helsinki Design Lab, a design team within the Finnish Innovation Fund focused on policy issues like carbon reduction, education, welfare services, and economic development. His career began in technology, designing and programming user interfaces for early-stage startups. Boyer has published works including LEAP Dialogues: Career Pathways in Design for Social Innovation, Brickstarter, Helsinki Street Eats, Legible Practices, and In Studio: Recipes For Systemic Change. During 2019-2020, he served as the Eliel Saarinen Visiting Assistant Professor of Practice at the University of Michigan Taubman College. He also serves on the board of directors for Public Policy Lab in New York City and is based in Detroit, MI.

Research topics

  • Pediatrics
  • Medicine
  • Demography
  • Environmental health

Selected publications

  • Racial and ethnic disparities of sudden unexpected infant death in large US cities: a descriptive epidemiological study

    Injury Epidemiology · 2022 · 28 citations

    1st authorCorresponding
    • Demography
    • Medicine
    • Environmental health

    BACKGROUND: Sudden unexpected infant death (SUID) accounts for ~ 3400 deaths per year in the USA, and minimal progress has been made in reducing SUID over the past two decades. SUID is the sudden death of an infant that has occurred as a result of accidental suffocation in a sleeping environment, SIDS (sudden infant death syndrome), or from an unknown cause of death. Nationally, non-Hispanic Black (NHB) infants have twice the risk of SUID compared to non-Hispanic White (NHW) infants. In Chicago, this disparity is greatly magnified. To explore whether this disparity is similarly seen in other large cities, we analyzed SUIDs by race and ethnicity for a seven-year period from the 10 most populous US cities. SUID case counts by race and ethnicity were obtained for 2011-2017 from the 10 most populous US cities based on 2010 census data. For each city, we calculated average annual SUID rates (per 1000 live births) by race and ethnicity, allowing calculation of disparity rate ratios. FINDINGS: Nationally, from 2011 through 2017, there were 0.891 SUIDs per 1000 live births, with a rate of 0.847 for NHWs, 1.795 for NHBs, and 0.522 for Hispanics. In most study cities, the NHB and Hispanic SUID rates were higher than the corresponding national rate. Hispanic SUID rates were higher than NHW rates in 9 of the 10 largest cities. In every study city, the NHW SUID rate was lower than the national NHW rate. In Chicago, NHB infants had a SUID rate 12.735 times that of NHW infants. CONCLUSION: With few exceptions, the 10 largest US cities had higher NHB and Hispanic SUID rates, but lower NHW SUID rates, compared to the corresponding rates at the national level. Unlike the national pattern, Hispanic SUID rates were higher than NHW rates in 9 of the 10 largest cities. Prevention is currently hampered by the lack of detailed, accurate, and timely information regarding the circumstances of these tragic deaths. A national SUID surveillance system would allow greater understanding of the factors that lead to this disproportionately distributed and enduring cause of infant death.

  • Role of signalling molecules in behaviours mediated by the δ opioid receptor agonist SNC80

    British Journal of Pharmacology · 2017-12-26 · 36 citations

    articleOpen access

    Background and Purpose GPCRs exist in multiple conformations that can engage distinct signalling mechanisms which in turn may lead to diverse behavioural outputs. In rodent models, activation of the δ opioid receptor (δ‐receptor) has been shown to elicit antihyperalgesia, antidepressant‐like effects and convulsions. We recently showed that these δ‐receptor‐mediated behaviours are differentially regulated by the GTPase‐activating protein regulator of G protein signalling 4 (RGS4), which facilitates termination of G protein signalling. To further evaluate the signalling mechanisms underlying δ‐receptor‐mediated antihyperalgesia, antidepressant‐like effects and convulsions, we observed how changes in Gα o or arrestin proteins in vivo affected behaviours elicited by the δ‐receptor agonist SNC80 in mice. Experimental Approach Transgenic mice with altered expression of various signalling molecules were used in the current studies. Antihyperalgesia was measured in a nitroglycerin‐induced thermal hyperalgesia assay. Antidepressant‐like effects were evaluated in the forced swim test. Mice were also observed for convulsive activity following SNC80 treatment. Key Results In Gα o RGS‐insensitive heterozygous knock‐in mice, the potency of SNC80 to produce antihyperalgesia and antidepressant‐like effects was enhanced with no change in SNC80‐induced convulsions. Conversely, in Gα o heterozygous knockout mice, SNC80‐induced antihyperalgesia was abolished while antidepressant‐like effects and convulsions were unaltered. No changes in SNC80‐induced behaviours were observed in arrestin 3 knockout mice. SNC80‐induced convulsions were potentiated in arrestin 2 knockout mice. Conclusions and Implications Taken together, these findings suggest that different signalling molecules may underlie the convulsive effects of the δ‐receptor relative to its antihyperalgesic and antidepressant‐like effects.

  • <i>In vivo</i> characterization of the novel delta opioid receptor positive allosteric modulator BMS‐986187

    The FASEB Journal · 2017-04-01 · 1 citations

    article

    The delta opioid receptor (DOPr) is a member of the opioid receptor family of G protein‐coupled receptors (GPCR). Activation of DOPr induces antinociception, antihyperalgesia, and antidepressant‐like effects in animal models. However, some DOPr agonists cause convulsions, hindering their development as therapeutics in humans. Positive allosteric modulators (PAMs) bind to a receptor site distinct from the orthosteric binding site of a GPCR and may have several advantages over orthosteric agonists including greater selectivity, a larger safety margin and preservation of the spatiotemporal integrity of the endogenous system. Therefore, a PAM could be an effective strategy for eliciting DOPr‐mediated therapeutic effects without convulsions. To evaluate this hypothesis, we investigated the ability of the DOPr PAM BMS‐986187 to elicit DOPr‐mediated behaviors in mice alone or in combination with the DOPr orthosteric agonist SNC80. DOPr‐mediated antinociception was assessed in the acetic acid‐induced stretch assay. Antihyperalgesia was evaluated using a nitroglycerin‐induced thermal hyperalgesia assay. Antidepressant‐like effects were measured using the forced swim test. BMS‐986187 enhanced the potency of SNC80 to induce antinociception and antihyperalgesia without altering SNC80‐induced convulsions. BMS‐986187 alone produced antidepressant‐like effects without convulsions. These antidepressant‐like effects were blocked by the DOPr antagonist naltrindole and absent in DOPr knockout mice, indicating a DOPr‐mediated effect. Pretreatment with the enkephalinase inhibitor RB101 produced a synergistic effect in the forced swim test with BMS‐986187 but not SNC80 suggesting that BMS‐986187 exerts it antidepressant‐like effects by enhancing the actions of endogenous enkephalins. Overall, these findings suggest that BMS‐986187 functionally increases the therapeutic index of SNC80 and that a DOPr PAM could be a safer alternative to an orthosteric agonist as a novel treatment for depression. Support or Funding Information This project was partially funded by a PhRMA Foundation Starter Grant to EMJ and by NIH Grant DA035316 to JRT.

  • The behavioral effects of a mixed efficacy antinociceptive peptide, VRP26, following chronic administration in mice

    Psychopharmacology · 2016-04-27 · 20 citations

    articleOpen access
  • A Centrally Active, Peripherally Available Mixed Efficacy MOR/DOR Ligand that Displays Reduced Development of Negative Side Effects

    The FASEB Journal · 2016-04-01

    article

    Mu‐opioid receptor (MOR) agonists have long been used in the treatment of pain and are currently the gold standard for pain management in the clinic. While these compounds produce considerable analgesia, their use produces many adverse effects, such as the development of antinociceptive tolerance, physical dependence, euphoria, and constipation. It has been suggested that the co‐administration of a MOR agonist with a delta opioid receptor (DOR) antagonist may produce MOR‐mediated analgesia with reduced side effects. However, administering drug cocktails has considerable complications related to potential diverse pharmacokinetic properties of the two chemical entities. We therefore explored the development of multifunctional ligands that display both MOR agonism and DOR antagonism in a single molecule. We have previously reported a cyclic peptide with a C‐terminal β‐glucoserine, VRP26, which displays the desired MOR agonist/DOR antagonist profile in vitro and produces opioid mediated antinociception in the warm water tail withdrawal assay after peripheral administration in male C57BL/6N mice. The goals of the current study were to evaluate whether VRP26: 1) crosses the blood brain barrier and 2) produces tolerance, dependence, rewarding effects, and constipation. The effects of VRP26 on centrally‐mediated behaviors in nitroglycerin‐induced hyperalgesia assay and the tail suspension test were evaluated. Tolerance and dependence were evaluated following continuous VRP26 infusion for 7 days, rewarding effects were evaluated in a conditioned place preference assay, and constipation was evaluated by fecal bolus production following acute drug administration. VRP26 reversed nitroglycerin‐induced hyperalgesia and attenuated antidepressant‐like effects induced by the DOR agonist SNC80. Unlike fentanyl, 7 day continuous administration of VRP26 failed to produce a rightward shift in the antinociceptive dose response curve and produced fewer signs of naltrexone‐precipitated withdrawal than fentanyl. VRP26, unlike fentanyl, did not produce significant conditioned place preference. VRP26 also was less potent that morphine in producing constipating effects. In conclusion, VRP26 produces centrally mediated antinociception, with limited development of antinociceptive tolerance, physical dependence, and rewarding effects. Further, VRP26 has a greater therapeutic index between antinociceptive and constipating effects, demonstrating potential increased tolerability. VRP26 demonstrates proof of concept that mixed efficacy opioid ligands may be better alternatives to traditional opioid analgesics for chronic pain management, producing pain relief with limited negative effects. Support or Funding Information This work was funded by NIH Grant DA003910. J.P.A was supported by the National Institutes of Health under Ruth L. Kirschstein National Research Service Award T32 DA007267. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH.

Frequent coauthors

  • Emily M. Jutkiewicz

    University of Michigan–Ann Arbor

    4 shared
  • Isaac Dripps

    University of Illinois Chicago

    3 shared
  • Henry I. Mosberg

    University of Michigan–Ann Arbor

    2 shared
  • John R. Traynor

    University of Michigan–Ann Arbor

    2 shared
  • Jessica P. Anand

    University of Michigan–Ann Arbor

    2 shared
  • Kenner C. Rice

    National Institute on Alcohol Abuse and Alcoholism

    1 shared
  • Richard R. Neubig

    Michigan State University

    1 shared
  • Douglas R. Roehler

    National Center for Injury Prevention and Control

    1 shared
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