About

Bruce Robinson is a Clinical Assistant Professor of General Dentistry at the Henry M. Goldman School of Dental Medicine, Boston University. He earned his DDS degree from Georgetown University in 1978. Based at the dental school's Office 635 Albany Street, G-355, he is involved in teaching and clinical practice within the Department of General Dentistry. His professional focus includes general dentistry, emphasizing preventive and restorative dental care, and he contributes to the education of students in these areas. Robinson's role involves providing state-of-the-art dental care through the school's teaching clinic and faculty practice, supporting the institution's mission to deliver comprehensive dental services and education.

Research topics

• Pharmacology
• Internal medicine
• Pathology
• Medicine

Selected publications

• Renin-Angiotensin System Modulation With Synthetic Angiotensin (1-7) and Angiotensin II Type 1 Receptor–Biased Ligand in Adults With COVID-19

  JAMA · 2023 · 50 citations

  Senior authorCorresponding
  • Medicine
  • Internal medicine
  • Pharmacology

  Importance: Preclinical models suggest dysregulation of the renin-angiotensin system (RAS) caused by SARS-CoV-2 infection may increase the relative activity of angiotensin II compared with angiotensin (1-7) and may be an important contributor to COVID-19 pathophysiology. Objective: To evaluate the efficacy and safety of RAS modulation using 2 investigational RAS agents, TXA-127 (synthetic angiotensin [1-7]) and TRV-027 (an angiotensin II type 1 receptor-biased ligand), that are hypothesized to potentiate the action of angiotensin (1-7) and mitigate the action of the angiotensin II. Design, Setting, and Participants: Two randomized clinical trials including adults hospitalized with acute COVID-19 and new-onset hypoxemia were conducted at 35 sites in the US between July 22, 2021, and April 20, 2022; last follow-up visit: July 26, 2022. Interventions: A 0.5-mg/kg intravenous infusion of TXA-127 once daily for 5 days or placebo. A 12-mg/h continuous intravenous infusion of TRV-027 for 5 days or placebo. Main Outcomes and Measures: The primary outcome was oxygen-free days, an ordinal outcome that classifies a patient's status at day 28 based on mortality and duration of supplemental oxygen use; an adjusted odds ratio (OR) greater than 1.0 indicated superiority of the RAS agent vs placebo. A key secondary outcome was 28-day all-cause mortality. Safety outcomes included allergic reaction, new kidney replacement therapy, and hypotension. Results: Both trials met prespecified early stopping criteria for a low probability of efficacy. Of 343 patients in the TXA-127 trial (226 [65.9%] aged 31-64 years, 200 [58.3%] men, 225 [65.6%] White, and 274 [79.9%] not Hispanic), 170 received TXA-127 and 173 received placebo. Of 290 patients in the TRV-027 trial (199 [68.6%] aged 31-64 years, 168 [57.9%] men, 195 [67.2%] White, and 225 [77.6%] not Hispanic), 145 received TRV-027 and 145 received placebo. Compared with placebo, both TXA-127 (unadjusted mean difference, -2.3 [95% CrI, -4.8 to 0.2]; adjusted OR, 0.88 [95% CrI, 0.59 to 1.30]) and TRV-027 (unadjusted mean difference, -2.4 [95% CrI, -5.1 to 0.3]; adjusted OR, 0.74 [95% CrI, 0.48 to 1.13]) resulted in no difference in oxygen-free days. In the TXA-127 trial, 28-day all-cause mortality occurred in 22 of 163 patients (13.5%) in the TXA-127 group vs 22 of 166 patients (13.3%) in the placebo group (adjusted OR, 0.83 [95% CrI, 0.41 to 1.66]). In the TRV-027 trial, 28-day all-cause mortality occurred in 29 of 141 patients (20.6%) in the TRV-027 group vs 18 of 140 patients (12.9%) in the placebo group (adjusted OR, 1.52 [95% CrI, 0.75 to 3.08]). The frequency of the safety outcomes was similar with either TXA-127 or TRV-027 vs placebo. Conclusions and Relevance: In adults with severe COVID-19, RAS modulation (TXA-127 or TRV-027) did not improve oxygen-free days vs placebo. These results do not support the hypotheses that pharmacological interventions that selectively block the angiotensin II type 1 receptor or increase angiotensin (1-7) improve outcomes for patients with severe COVID-19. Trial Registration: ClinicalTrials.gov Identifier: NCT04924660.

  DOI

• Early Identification of Acute Lung Injury in a Porcine Model of Hemorrhagic Shock

  Journal of Surgical Research · 2019-10-24 · 7 citations

  article
  PublisherDOI

• 1736: ANTITHROMBIN III AND ANTI-XA IMPACT ON ENOXAPARIN CHEMOPROPHYLAXIS IN HIGH-RISK TRAUMA PATIENTS

  Critical Care Medicine · 2018-12-18

  article

  Droege, Molly1; Droege, Chris1; Webb, Megan2; Philpott, Carolyn3; Ernst, Neil4; Athota, Krishna5; Wakefield, Devin6; Dowd, Joseph6; Gomaa, Dina4; Robinson, Bryce7; Hanseman, Dennis5; Elterman, Joel4; Mueller, Eric4 Author Information

  PublisherDOI

• 1108

  Critical Care Medicine · 2015-11-14 · 1 citations

  article

  Welch, Megan; Droege, Molly; Droege, Chris; Ernst, Neil; Keegan, Shaun; Robinson, Bryce; Mueller, Eric

  PublisherDOI

• The Massive Transfusion Score as a decision aid for resuscitation

  The Journal of Trauma: Injury, Infection, and Critical Care · 2015-10-30 · 39 citations

  articleOpen access

  BACKGROUND: Previous work proposed a Massive Transfusion Score (MTS) calculated from values obtained in the emergency department to predict likelihood of massive transfusion (MT). We hypothesized the MTS could be used at Hour 6 to differentiate who continues to require balanced resuscitation in Hours 7 to 24 and to predict death at 28 days. METHODS: We prospectively enrolled patients in whom the MT protocol was initiated from 2005 to 2011. Data including timing of blood products were determined at Hours 0, 6, 12, and 24. For each patient, transfusion needs were defined based on either an inappropriately low hemoglobin response to transfusion or a hemoglobin decrease of greater than 1 g/dL if no transfusion. Timing and cause of death were used to account for survivor bias. Multivariate logistic regression was used to determine independent predictors of outcome. RESULTS: A total of 190 MT protocol activations were included, and by Hour 6, 61% required 10 U or greater packed red blood cells. Calculated at initial presentation, a revised MTS (systolic blood pressure < 90 mm Hg, base deficit ≥ 6, temperature < 35.5°C, international normalized ratio > 1.5, hemoglobin < 11 g/dL) was superior to the original MTS (including heart rate ≥ 120 beats per minute, Focused Assessment With Sonography in Trauma [FAST] status, mechanism) or the Assessment of Blood Consumption (ABC) score for predicting MT (area under the curve [AUC] MT at 6 hours, 0.68; 95% confidence interval [CI], 0.57-0.79; at 24 hours, 0.72; 0.61-0.83; p < 0.05). For those alive at Hour 6, the revised MTS was predictive of future packed red blood cell need (AUC, 0.87) in Hours 7 to 12, 24-hour mortality (AUC, 0.95), and 28-day mortality (AUC, 0.77). For each additional positive trigger of the MTS at Hour 6, the odds of death at 24 hours and 28 days were substantially increased (24-hour odds ratio, 4.6; 95% CI, 2.3-9.3; 28-day odds ratio, 2.2; 95% CI, 1.5-3.2; p < 0.0001). CONCLUSION: Early end points of resuscitation adopted from the components of the revised MTS are predictive of ongoing transfusion. Failure to normalize these components by Hour 6 portends a particularly poor prognosis. LEVEL OF EVIDENCE: Prognostic study, level 3.

  PublisherOA PDFDOI

• Substance P Mediates Reduced Pneumonia Rates After Traumatic Brain Injury

  Critical Care Medicine · 2014-07-11 · 24 citations

  articleOpen access

  OBJECTIVES: Traumatic brain injury results in significant morbidity and mortality and is associated with infectious complications, particularly pneumonia. However, whether traumatic brain injury directly impacts the host response to pneumonia is unknown. The objective of this study was to determine the nature of the relationship between traumatic brain injury and the prevalence of pneumonia in trauma patients and investigate the mechanism of this relationship using a murine model of traumatic brain injury with pneumonia. DESIGN: Data from the National Trauma Data Bank and a murine model of traumatic brain injury with postinjury pneumonia. SETTING: Academic medical centers in Cincinnati, OH, and Boston, MA. PATIENTS/SUBJECTS: Trauma patients in the National Trauma Data Bank with a hospital length of stay greater than 2 days, age of at least 18 years at admission, and a blunt mechanism of injury. Subjects were female ICR mice 8-10 weeks old. INTERVENTIONS: Administration of a substance P receptor antagonist in mice. MEASUREMENTS AND MAIN RESULTS: Pneumonia rates were measured in trauma patients before and after risk adjustment using propensity scoring. In addition, survival and pulmonary inflammation were measured in mice undergoing traumatic brain injury with or without pneumonia. After risk adjustment, we found that traumatic brain injury patients had significantly lower rates of pneumonia compared to blunt trauma patients without traumatic brain injury. A murine model of traumatic brain injury reproduced these clinical findings with mice subjected to traumatic brain injury demonstrating increased bacterial clearance and survival after induction of pneumonia. To determine the mechanisms responsible for this improvement, the substance P receptor was blocked in mice after traumatic brain injury. This treatment abrogated the traumatic brain injury-associated increases in bacterial clearance and survival. CONCLUSIONS: The data demonstrate that patients with traumatic brain injury have lower rates of pneumonia compared to non-head-injured trauma patients and suggest that the mechanism of this effect occurs through traumatic brain injury-induced release of substance P, which improves innate immunity to decrease pneumonia.

  PublisherOA PDFDOI

• 235

  Critical Care Medicine · 2012-12-01

  article

  Introduction: Delirium is a fluctuating disturbance in consciousness associated with increased mortality. Severely injured soldiers represent a unique population due to their age and injury mechanism. Our purpose was to discern the prevalence of delirium in this unstudied population. Hypothesis: We hypothesized delirium would be common due to high injury severity scores (ISS) and frequent use of multidrug sedation regimens. Methods: Screening for delirium using the confusion assessment method (CAM-ICU) was initiated at Craig Joint Theater Hospital in Bagram, Afghanistan (CJTH) for all patients admitted to the ICU. Data was compiled, capturing the first fifty English speaking trauma patients with documented CAM-ICU score. Results: From July 22 - August 23, 2012, 104 patients were admitted to the ICU, including fifty English speaking trauma patients. All were male, mean age of 27.8 years. Ninety-two percent were of US origin and 88% were US military personnel. Most common injury mechanisms were blast (68%) and gunshot wounds (26%). Sixty-five percent of blast injuries occurred while patients were dismounted. Mean ISS was 20, and average ICU length of stay at CJTH was 2.3 days. Sixty-four percent of patients were ventilated for an average of 1.2 days. CAM-ICU scores were initiated upon admission to the ICU. Average time from injury to first CAM assessment was 25 hours and average time from hospital admission to CAM assessment was 7 hours. Overall, delirium was present in 44% of patients, 36% at first CAM assessment. Most patients received Fentanyl for pain control (62%) and Propofol for sedation (52%). Ketamine was used in 16% of patients and 8% had either an epidural or peripheral nerve catheter. There was no relationship between delirium and mechanism of injury (p=0.5) or use of Ketamine on first ICU day (p=.2262). An increased number of vent days was associated with delirium (p<.0001) and admission mechanical ventilation with admission delirium (p=.0025). Conclusions: This study demonstrates a high rate of delirium in this unique population. Additional study is needed to elucidate the causes of delirium in this population so appropriate preventative steps and treatment algorithms can be developed.

  PublisherDOI

Frequent coauthors

• Dennis J. Hanseman

  University of Cincinnati

  18 shared

• Timothy A. Pritts

  University of Cincinnati

  17 shared

• Michael D. Goodman

  University of Cincinnati

  17 shared

• Daniel G. Remick

  Boston University

  16 shared

• Charles C. Caldwell

  University of Cincinnati Medical Center

  16 shared

• Michael W. Cripps

  University of Colorado Anschutz Medical Campus

  16 shared

• Alex B. Lentsch

  University of Cincinnati

  16 shared

• Mary F. Nelson

  University of Utah

  16 shared

Education

• Other

  Georgetown University

  1978