About

Robert Taylor is a Professor of Conducting and the Director of Bands at Northwestern University, where he holds the John W. Beattie Chair of Music. He has a career spanning over thirty years in music education, with previous appointments including the University of British Columbia, University of Puget Sound, and Eureka High School. Taylor conducts the Symphonic Wind Ensemble, teaches graduate and undergraduate conducting, and leads all aspects of the band program at Northwestern. He is known for innovative and immersive concert programming and maintains an active schedule as a guest conductor, having performed with various orchestras and contemporary music groups. His collaborations include virtuosi performers, composers, and crossover artists from diverse musical backgrounds. Taylor is a passionate advocate for music education, frequently serving as a festival adjudicator, rehearsal clinician, and guest conductor across North America and internationally, including serving as principal conductor of the Puget Sound Youth Wind Ensemble and guest conductor of numerous honor groups worldwide. He holds a Master of Music and Doctor of Music degrees in conducting from Northwestern University, where he studied with Mallory Thompson, and a Bachelor of Arts in Trumpet and Music Education from Humboldt State University. His research focuses on wind literature, rehearsal techniques, integration of technology, and the application of Ashtanga Yoga to improve body awareness and injury prevention in musicians and conductors. Taylor has contributed to numerous publications, co-authored 'The Horizon Leans Forward,' and has been recognized with awards such as the Killam Laureate, Jacob K. Javits Fellow, and Thomas A. Davis Teaching Prize. He has served on executive boards of music education organizations and is a member of several professional societies.

Research topics

• Pathology
• Virology
• Medicine
• Biology
• Immunology
• Internal medicine
• Genetics
• Mathematics

Selected publications

• PET/CT Targeted Tissue Sampling Reveals Intravenously Administered HGN194 IgG1 Affects HIV Distribution after Rectal Exposure

  AIDS Research and Human Retroviruses · 2024 · 1 citations

  1st authorCorresponding
  • Medicine
  • Pathology
  • Virology

  Cu-labeled, photoactivatable-green fluorescent protein HIV (PA-GFP-BaL) and fluorescently labeled HGN194 IgG1 to determine whether intravenously instilled IgG influences viral interaction with mucosal barriers and viral penetration in colorectal tissue 2 h after rectal viral challenge. Our results show that IgG1 did not alter the number of virions found throughout the colon or viral penetration into the epithelium of the rectum or descending colon. A minor increase in virions was observed in the transverse colon of IgG1 treated animals. Overall, the number of viral particles found in the mesenteric lymph nodes was low. However, IgG1 administration resulted in a significant reduction of virions found in mesenteric lymph nodes. Taken together, our results show that HGN194 IgG1 does not prevent virions from penetrating into the colorectal mucosa but may perturb HIV virion access to the lymphatic system.

  PublisherOA PDFDOI

• PET/CT targeted tissue sampling reveals virus specific dIgA can alter the distribution and localization of HIV after rectal exposure

  PLoS Pathogens · 2021 · 15 citations

  1st authorCorresponding
  • Biology
  • Virology
  • Immunology

  Human immunodeficiency virus (HIV) vaccines have not been successful in clinical trials. Dimeric IgA (dIgA) in the form of secretory IgA is the most abundant antibody class in mucosal tissues, making dIgA a prime candidate for potential HIV vaccines. We coupled Positron Emission Tomography (PET) imaging and fluorescent microscopy of 64Cu-labeled, photoactivatable-GFP HIV (PA-GFP-BaL) and fluorescently labeled dIgA to determine how dIgA antibodies influence virus interaction with mucosal barriers and viral penetration in colorectal tissue. Our results show that HIV virions rapidly disseminate throughout the colon two hours after exposure. The presence of dIgA resulted in an increase in virions and penetration depth in the transverse colon. Moreover, virions were found in the mesenteric lymph nodes two hours after viral exposure, and the presence of dIgA led to an increase in virions in mesenteric lymph nodes. Taken together, these technologies enable in vivo and in situ visualization of antibody-virus interactions and detailed investigations of early events in HIV infection.

  PublisherDOI

• Localization of infection in neonatal rhesus macaques after oral viral challenge

  bioRxiv (Cold Spring Harbor Laboratory) · 2021-07-30 · 2 citations

  preprintOpen access1st author

  Abstract While vertical transmission of human immunodeficiency virus (HIV) can occur in utero and during delivery and through breastfeeding. We utilized Positron Emission Tomography (PET) imaging coupled with fluorescent microscopy of 64 Cu-labeled photoactivatable-GFP-HIV (PA-GFP-BaL) to determine how HIV virions distribute and localize in neonatal rhesus macaques two and four hours after oral viral challenge. Our results show that by four hours after oral viral exposure, HIV virions localize to and penetrate the rectal mucosa. We also used a dual viral challenge with a non-replicative viral vector and a replication competent SHIV-1157ipd3N4 to examine viral transduction and dissemination at 96 hours. Our data show that while SHIV-1157ipd3N4 infection can be found in the oral cavity and upper gastrointestinal (GI) tract, the small and large intestine contained the largest number of infected cells. Moreover, we found that T cells were the biggest population of infected immune cells. Thus, thanks to these novel technologies, we are able to visualize and delineate of viral distribution and infection throughout the entire neonatal GI tract during acute viral infection. Author Summary Approximately 1.8 million children are currently living with human immunodeficiency virus (HIV). While mother-to-child HIV transmission can occur in utero and during delivery, it most commonly occurs through breastfeeding, creating the need to understand how the virus moves throughout the body and infects the infant once breast milk is consumed. Here, we used multiple imaging techniques and PCR to determine how HIV distributes throughout the gastrointestinal tract after oral viral exposure and in which tissues and cell types become acutely infected. We found that HIV rapidly spreads throughout and penetrates the entire gastrointestinal tract as early as four hours after exposure. We also found that the intestine contained the largest number of infected cells at 96 hours and that most cells infected were T cells. Our study shows that these imaging technologies allow for the examination of viral distribution and infection in a rhesus macaque model.

  PublisherOA PDFDOI

• Localization of infection in neonatal rhesus macaques after oral viral challenge

  PLoS Pathogens · 2021 · 7 citations

  1st authorCorresponding
  • Virology
  • Biology
  • Immunology

  Vertical transmission of human immunodeficiency virus (HIV) can occur in utero, during delivery, and through breastfeeding. We utilized Positron Emission Tomography (PET) imaging coupled with fluorescent microscopy of 64Cu-labeled photoactivatable-GFP-HIV (PA-GFP-BaL) to determine how HIV virions distribute and localize in neonatal rhesus macaques two and four hours after oral viral challenge. Our results show that by four hours after oral viral exposure, HIV virions localize to and penetrate the rectal mucosa. We also used a dual viral challenge with a non-replicative viral vector and a replication competent SHIV-1157ipd3N4 to examine viral transduction and dissemination at 96 hours. Our data show that while SHIV-1157ipd3N4 infection can be found in the oral cavity and upper gastrointestinal (GI) tract, the small and large intestine contained the largest number of infected cells. Moreover, we found that T cells were the biggest population of infected immune cells. Thus, thanks to these novel technologies, we are able to visualize and delineate of viral distribution and infection throughout the entire neonatal GI tract during acute viral infection.

  PublisherDOI

• PET/CT targeted tissue sampling reveals virus specific dIgA can alter the distribution and localization of HIV after rectal exposure

  bioRxiv (Cold Spring Harbor Laboratory) · 2020-12-24

  preprintOpen access1st author

  Abstract HIV vaccines have not been successful in clinical trials. Dimeric IgA (dIgA) is the most abundant antibody class in mucosal tissues, making dIgA a prime candidate for potential HIV vaccines. We coupled Positron Emission Tomography (PET) imaging and fluorescent microscopy of 64 Cu-labeled, photoactivatable-GFP HIV (PA-GFP-BaL) and fluorescently labeled dIgA to determine how dIgA antibodies influence virus interaction with mucosal barriers and viral penetration in colorectal tissue. Our results show that HIV virions rapidly disseminate throughout the colon two hours after exposure. The presence of dIgA resulted in an increase in virions and penetration depth in the transverse colon. Moreover, virions were found in the mesenteric lymph nodes two hours after viral exposure, and the presence of dIgA led to an increase in virions in mesenteric lymph nodes. Taken together, these technologies enable in vivo and in situ visualization of antibody-virus interactions and detailed investigations of early events in HIV infection.

  PublisherOA PDFDOI

• Abstract TP351: Axl/Mer Receptor Tyrosine Kinase Mediates Erythrophagocytosis-Induced Macrophage Reparative Phenotype and Brain Recovery in Experimental Intracerebral Hemorrhage

  Stroke · 2017-02-01

  article

  Introduction: Local inflammation contributes to both brain injury and recovery after intracerebral hemorrhage (ICH). Our previous studies have shown brain-infiltrating macrophages (BIMs) aggravate early brain injury after ICH; however, BIMs increase scavenger receptor CD36 levels over time, and hematoma clearance is delayed in the absence of BIMs. The mechanism that mediates BIMs phenotypic change in the ICH brain is elusive. In this study, we delineate the dynamic transcriptome profile of BIMs after ICH and test potential mediator that might modulate BIMs polarity in ICH. Methods: Autologous blood injection ICH model and thrombin-treated bone marrow-derived macrophages (BMDM) were used to mimic ICH in vivo and in vitro . BIMs were isolated by FACS, and the 780 transcriptome of BIMs were determined using NanoString. Flow cytometry and RT-qPCR were performed to detect the frequency of phosphatidylserine-positive (eryptotic) RBCs and to assess BIMs phenotype in the perihematomal tissue. Erythrophagocytosis of eryptotic RBCs was identified by immunofluorescence and microscopy. Neurologic deficit was evaluated by cylinder test. Axl/Mer receptor tyrosine kinase double knockout (AM DKO) mice, AM DKO bone-marrow chimeras, and AM DKO BMDM were used to evaluate the function of Axl/Mer on macrophage phenotype and on brain recovery after ICH. Results: BIMs highly expressed proinflammatory transcripts such as cd86 , tlr2 , nlrp3 , and tnf at days 1 and 3 post-ICH; these were decreased at days 7 and 10. Transcripts relevant to efferocytosis ( axl ) and lysosome formation ( cd63 ) increased from days 3 to 10 post-ICH. At days 1 and 3, phosphatidylserine levels was increased on RBCs in the ICH brain. Engulfment of eryptotic RBCs reduced proinflammatory phenotype of BMDM. Thrombin-stimulated AM DKO BMDM had reduced erythrophagocytosis ability and increased tnf and il-6 gene expression. AM DKO mice and AM DKO chimeras had low CD36 and high MHC II levels on BIMs and had worse functional outcome after ICH. Conclusions: BIMs initially express proinflammatory phenotype and then switch to a reparative phenotype after ICH. Axl/Mer is involved in regulation of macrophage polarity through modulating erythrophagocytosis ability and contributes to ICH brain recovery.

  PublisherDOI

• Microglial Responses in Recovery after Intracerebral Hemorrhage

  OpenCommons - UConn (University of Connecticut) · 2016-01-01

  article1st authorCorresponding

  Intracerebral hemorrhage (ICH) is a devastating subset of stroke that has a high mortality rate and no specific treatment. ICH results from the rupture of blood vessels within the brain, leading to microglial activation. Upon activation, microglia can polarize into many phenotypes ranging from pro-inflammatory to a phenotype associated with wound healing and repair. Using bone marrow chimeras, we studied the role of CX3CR1 independently on monocytes and microglia. We found that CX3CR1 on Ly6Clo monocytes is dispensable after ICH. Interestingly, Ly6Clo monocytes enter the brain parenchyma independently of CX3CR1 expression. We utilized the CX3CR1-regulation of microglial activation to study microglial responses after ICH. We found that microglial dysregulation leads to poor functional outcomes and a reduction in TGF-β1 gene expression. Through unbiased transcriptional analysis, we found that microglia transition from a pro-inflammatory phenotype to a phenotype that promotes wound healing and repair; this transition is likely mediated by TGF-β1. In vitro, TGF-β1 decreased microglial pro-inflammatory gene expression and TNF production. In vivo, TGF-β1 improved functional outcomes at 24 hours after ICH and decreased microglial IL-6 gene expression. Furthermore, patients who increased plasma TGF-β1 concentrations from 6 to 72 hours after ICH had better outcomes at 90 days. We investigated whether microglia aid in repair by phagocytosing myelin debris after ICH. In vivo, myeloid cells phagocytose myelin 7 days after ICH. In vitro, microglia phagocytose myelin, which resulted in a decrease in pro-inflammatory gene expression. Taken together, our data suggest that TGF-β1 modulates microglial-mediated neuroinflammation and promotes functional recovery after ICH. Our data also suggests that microglia aid in recovery after ICH through the phagocytosis of myelin debris and that phagocytosis quells microglial pro-inflammatory responses.

  Publisher

• TGF-β1 modulates microglial phenotype and promotes recovery after intracerebral hemorrhage

  Journal of Clinical Investigation · 2016-11-27 · 278 citations

  articleOpen access1st author

  Intracerebral hemorrhage (ICH) is a devastating form of stroke that results from the rupture of a blood vessel in the brain, leading to a mass of blood within the brain parenchyma. The injury causes a rapid inflammatory reaction that includes activation of the tissue-resident microglia and recruitment of blood-derived macrophages and other leukocytes. In this work, we investigated the specific responses of microglia following ICH with the aim of identifying pathways that may aid in recovery after brain injury. We used longitudinal transcriptional profiling of microglia in a murine model to determine the phenotype of microglia during the acute and resolution phases of ICH in vivo and found increases in TGF-β1 pathway activation during the resolution phase. We then confirmed that TGF-β1 treatment modulated inflammatory profiles of microglia in vitro. Moreover, TGF-β1 treatment following ICH decreased microglial Il6 gene expression in vivo and improved functional outcomes in the murine model. Finally, we observed that patients with early increases in plasma TGF-β1 concentrations had better outcomes 90 days after ICH, confirming the role of TGF-β1 in functional recovery from ICH. Taken together, our data show that TGF-β1 modulates microglia-mediated neuroinflammation after ICH and promotes functional recovery, suggesting that TGF-β1 may be a therapeutic target for acute brain injury.

  PublisherOA PDFDOI

• Abstract TMP55: TGF-β1 Induces Microglial BDNF Production and Improves Functional Outcome After Intracerebral Hemorrhage

  Stroke · 2016-02-01 · 3 citations

  article1st authorCorresponding

  Introduction: Intracerebral hemorrhage (ICH) results in the activation of microglia. Microglia can become classically activated, promoting neurotoxicity or alternatively activated, promoting tissue repair. Our lab has previously shown that microglia become alternatively activated between 3 and 14 days after ICH. This transition is critical to recovery, yet the mechanism is unknown. The anti-inflammatory cytokine TGF-β1 has a critical role in microglial development and homeostasis. We hypothesize that TGF-β1 is the mediator of microglia alternative activation after ICH and that TGF-β1 promotes microglial secretion of BDNF to promote tissue repair. Methods: Primary microglial cultures from C57BL/6 (WT) P0-P2 pups were used to study the mechanism of alternative activation. Microglia were activated with thrombin with or without TGF-β1 for 8 and 24 hours. BDNF was measured by intracellular cytokine staining (ICS) (flow cytometry) and ELISA from cell supernatants. ICH was induced by injecting 25ul of whole blood into the right striatum of male WT mice. Mice were treated with either 10ng TGF-β1 or PBS intracerebrally immediately prior to blood injection to target microglia. Behavioral outcomes were measured by cylinder test and beam walking. Brains were harvested at 7 days for immunohistochemistry (IHC). Results: Primary microglia that were activated with thrombin and TGF-β1 had more BDNF+ cells by ICS at 8 hours and secreted more BDNF by ELISA at 24 hours compared to thrombin alone in vitro (fig 1). Mice treated with TGF-β1 had better functional outcomes by cylinder test and beam walking than PBS treated mice 24 hours after ICH. TGF-β1 treated mice had significantly more BDNF+ CD11b+ cells (microglia/macrophages) than PBS treated 7 days after ICH by IHC. Conclusions: TGF-β1 treatment induces microglial BDNF production and improves functional outcomes 24 hours after ICH. Ongoing work will determine whether microglial BDNF production is the link to improved outcomes.

  PublisherDOI

• Abstract TP257: Apoptotic Erythrocytes Attenuate Macrophages Proinflammatory Phenotype in Intracerebral Hemorrhage

  Stroke · 2016-02-01

  article

  Introduction: Inflammation contributes to both injury and recovery after intracerebral hemorrhage (ICH). Our previous studies showed that blood-derived CCR2 + monocytes/macrophages infiltration induces brain injury in acute ICH, whereas these cells are also essential for hematoma clearance at later stage of ICH. However, the mechanism that educates macrophages (MΦ) to change from classical activation to assisting in recovery in the hemorrhagic brain is still missing. In wound healing, contact with apoptotic cells induces macrophage alternative activation. Hypothesis: Apoptotic erythrocytes activate phosphatidylserine (PtdSer) receptors on MΦ to decrease MΦ proinflammatory response and induce MΦ alternative activation to aid in hematoma clearance. Methods: Bone marrow-derived macrophages were treated with thrombin to induce MΦ proinflammatory activation and to mimic ICH in vitro . We used PHK-26 labeled-apoptotic erythrocytes and recombinant annexin V to competitively inhibit PtdSer-receptor interactions to study the effect of apoptotic erythrocytes on MΦ phenotype and erythrophagocytosis ability. RT-qPCR and immunofluorescence were performed to detect MΦ polarization genes expression and the engulfment of erythrocytes. Results: Exposure to apoptotic erythrocytes decreased proinflammatory genes TNF-alpha (∼50%) and CD86 (∼30%) up-regulation induced by thrombin (10 U/ml) treatment for 12 hour (Figure). Recombinant annexin V (10μg) abolishes the benefit from apoptotic erythrocytes and reduces MΦ erythrophagocytosis. Conclusions: Macrophage alternative activation and erythrophagocytosis is induced by exposure to apoptotic erythrocytes in a PtdSer-dependent manner. Targeting PtdSer sensing receptor on MΦ could be a potential therapeutic strategy to promote MΦ alternative activation and subsequently to enhance hematoma clearance in ICH.

  PublisherDOI

Frequent coauthors

• Lauren Sansing

  Yale University

  26 shared

• Matthew D. Hammond

  Henry Ford Macomb Hospital

  19 shared

• Ruth M. Ruprecht

  Texas Biomedical Research Institute

  17 shared

• Youxi Ai

  Yale University

  16 shared

• Siqi Gong

  Texas Biomedical Research Institute

  11 shared

• Yanique Thomas

  5 shared

• Kenneth A. Rogers

  University of Louisiana at Lafayette

  5 shared

• Michael D. McRaven

  Northwestern University

  5 shared

Education

• B.A., Trumpet and Music Education

  Humboldt State University

• Other

  Northwestern University

  2002

• Other

  Northwestern University

  2006

Awards & honors

• Killam Laureate
• Jacob K. Javits Fellow
• Thomas A. Davis Teaching Prize