About

Professor Ravi Bapna is the Curtis L. Carlson Chair in Business Analytics and Information Systems and serves as the Academic Director of the Carlson Analytics Lab at the Carlson School of Management. He is closely affiliated with the Carlson School's MS in Business Analytics program and the Carlson Analytics Lab, where graduate students study a broad range of data analysis techniques and apply them to real business problems. These students are skilled in exploratory data visualization, predictive analytics techniques, programming, data engineering, machine learning methods, and more, emerging as data science professionals. Partner organizations have the opportunity to work with these talented students while supporting the educational mission of the programs. The faculty involved in the institute include scholars from across the Carlson School and beyond, bringing expertise in areas such as computer science, econometrics, strategy, and causal experimentation.

Research topics

• Physics
• Mechanics
• Environmental science
• Mathematics
• Geometry
• Thermodynamics
• Materials science
• Optics

Selected publications

• Supplementary Figure 3 from Liver Microvascular Injury and Thrombocytopenia of Antibody–Calicheamicin Conjugates in Cynomolgus Monkeys—Mechanism and Monitoring

  2023-03-31

  preprintOpen access

  <p>There were no significant PF-0259-related changes in IL-6 throughout the study. Data are represented as mean ratios to baseline {plus minus} 1 standard deviation (SD).</p>

  PublisherDOI

• Legends of supplementary figures from Liver Microvascular Injury and Thrombocytopenia of Antibody–Calicheamicin Conjugates in Cynomolgus Monkeys—Mechanism and Monitoring

  2023-03-31

  preprintOpen access

  <p>Legends of supplementary figures 1, 2 and 3</p>

  PublisherDOI

• Supplementary Figure 1 from Liver Microvascular Injury and Thrombocytopenia of Antibody–Calicheamicin Conjugates in Cynomolgus Monkeys—Mechanism and Monitoring

  2023-03-31

  preprintOpen access

  <p>PF-0259 did not induce platelet sequestration in kidney or lung. Monkeys were necropsied 48 hours after a single intravenous administration of vehicle or PF-0259 at 6 mg/m2. CD41 IHC for platelets was performed on kidney and lung samples from vehicle control (A and C, respectively) and PF-0259-dosed (B and D, respectively) monkeys. Contrary to what was observed in the liver, there was no increase in CD41 immunostaining and therefore no evidence of platelet sequestration in the kidney and lung vasculature following PF-0259 administration. Scale bar = 60 µm.</p>

  PublisherDOI

• Legends of supplementary figures from Liver Microvascular Injury and Thrombocytopenia of Antibody–Calicheamicin Conjugates in Cynomolgus Monkeys—Mechanism and Monitoring

  2023-03-31

  preprintOpen access

  <p>Legends of supplementary figures 1, 2 and 3</p>

  PublisherDOI

• Supplementary Figure 2 from Liver Microvascular Injury and Thrombocytopenia of Antibody–Calicheamicin Conjugates in Cynomolgus Monkeys—Mechanism and Monitoring

  2023-03-31

  preprintOpen access

  <p>PF-0259 did not induce platelet sequestration in spleen. Monkeys were dosed intravenously with vehicle or PF-0259 at 6 mg/m2/dose once every 3 weeks and were necropsied on Day 3 (at the time of platelet nadirs) or on Day 63 (at the end of the 3rd cycle). CD41 IHC for platelets was performed on spleen samples from vehicle control (A, C) and PF-0259-dosed (B, D) monkeys on Day 3 and Day 63. There was no evidence of increased CD41 immunostaining in PF-0259-dosed monkeys on Day 3 (B) or Day 63 (D) as compared with vehicle control monkeys (A and C, respectively), indicating lack of splenic sequestration of platelets at both time points. Noteworthy was a reduced CD41 immunostaining in PF-0259-dosed monkeys as compared with the control monkey on Day 3, indicating release of platelets from the spleen storage pool secondary to PF-0259-related acute thrombocytopenia. Scale bar = 60 µm.</p>

  PublisherDOI

• Supplementary Figure 1 from Liver Microvascular Injury and Thrombocytopenia of Antibody–Calicheamicin Conjugates in Cynomolgus Monkeys—Mechanism and Monitoring

  2023-03-31

  preprintOpen access

  <p>PF-0259 did not induce platelet sequestration in kidney or lung. Monkeys were necropsied 48 hours after a single intravenous administration of vehicle or PF-0259 at 6 mg/m2. CD41 IHC for platelets was performed on kidney and lung samples from vehicle control (A and C, respectively) and PF-0259-dosed (B and D, respectively) monkeys. Contrary to what was observed in the liver, there was no increase in CD41 immunostaining and therefore no evidence of platelet sequestration in the kidney and lung vasculature following PF-0259 administration. Scale bar = 60 µm.</p>

  PublisherDOI

• Data from Liver Microvascular Injury and Thrombocytopenia of Antibody–Calicheamicin Conjugates in Cynomolgus Monkeys—Mechanism and Monitoring

  2023-03-31

  preprintOpen access

  <div>Abstract<p><b>Purpose:</b> Adverse reactions reported in patients treated with antibody–calicheamicin conjugates such as gemtuzumab ozogamicin (Mylotarg) and inotuzumab ozogamicin include thrombocytopenia and sinusoidal obstruction syndrome (SOS). The objective of this experimental work was to investigate the mechanism for thrombocytopenia, characterize the liver injury, and identify potential safety biomarkers.</p><p><b>Experimental Design:</b> Cynomolgus monkeys were dosed intravenously at 6 mg/m<sup>2</sup>/dose once every 3 weeks with a nonbinding antibody–calicheamicin conjugate (PF-0259) containing the same linker-payload as gemtuzumab ozogamicin and inotuzumab ozogamicin. Monkeys were necropsied 48 hours after the first administration (day 3) or 3 weeks after the third administration (day 63).</p><p><b>Results:</b> PF-0259 induced acute thrombocytopenia (up to 86% platelet reduction) with nadirs on days 3 to 4. There was no indication of effects on megakaryocytes in bone marrow or activation of platelets in peripheral blood. Microscopic evaluation of liver from animals necropsied on day 3 demonstrated midzonal degeneration and loss of sinusoidal endothelial cells (SECs) associated with marked platelet accumulation in sinusoids. Liver histopathology on day 63 showed variable endothelial recovery and progression to a combination of sinusoidal capillarization and sinusoidal dilation/hepatocellular atrophy, consistent with early SOS. Among biomarkers evaluated, there were early and sustained increases in serum hyaluronic acid (HA) that correlated well with serum aspartate aminotransferase and liver microscopic changes, suggesting that HA may be a sensitive diagnostic marker of the liver microvascular injury.</p><p><b>Conclusions:</b> These data support the conclusion that target-independent damage to liver SECs may be responsible for acute thrombocytopenia (through platelet sequestration in liver sinusoids) and development of SOS. <i>Clin Cancer Res; 23(7); 1760–70. ©2016 AACR</i>.</p></div>

  PublisherDOI

• EFFECTS OF TIP CLEARANCE AND ROTATION ON THREE DIMENSIONAL FLOW FIELDS IN TURBINE CASCADES

  2023-01-01 · 1 citations

  articleSenior author

  The effect of tip clearance and rotation on the flow field in an annular turbine passage is studied numerically. Three-dimensional Navier-Stokes equations are solved with respect to the rotating frame of reference. The results indicate that the leakage flow through the tip gap induces a leakage vortex along the suction side of the blade. The leakage vortex interacts with the passage vortex and suppresses its development. Another vortex, referred as a tip vortex, at the edge between the tip and the pressure side of the blade is observed. With a larger gap, the strengthened leakage vortex pushes the passage vortex away from the suction side of the blade. With rotation, the leakage and passage vortex are pushed toward the suction side of the blade.

  PublisherDOI

• Supplementary Figure 3 from Liver Microvascular Injury and Thrombocytopenia of Antibody–Calicheamicin Conjugates in Cynomolgus Monkeys—Mechanism and Monitoring

  2023-03-31

  preprintOpen access

  <p>There were no significant PF-0259-related changes in IL-6 throughout the study. Data are represented as mean ratios to baseline {plus minus} 1 standard deviation (SD).</p>

  PublisherDOI

• Supplementary Figure 2 from Liver Microvascular Injury and Thrombocytopenia of Antibody–Calicheamicin Conjugates in Cynomolgus Monkeys—Mechanism and Monitoring

  2023-03-31

  preprintOpen access

  <p>PF-0259 did not induce platelet sequestration in spleen. Monkeys were dosed intravenously with vehicle or PF-0259 at 6 mg/m2/dose once every 3 weeks and were necropsied on Day 3 (at the time of platelet nadirs) or on Day 63 (at the end of the 3rd cycle). CD41 IHC for platelets was performed on spleen samples from vehicle control (A, C) and PF-0259-dosed (B, D) monkeys on Day 3 and Day 63. There was no evidence of increased CD41 immunostaining in PF-0259-dosed monkeys on Day 3 (B) or Day 63 (D) as compared with vehicle control monkeys (A and C, respectively), indicating lack of splenic sequestration of platelets at both time points. Noteworthy was a reduced CD41 immunostaining in PF-0259-dosed monkeys as compared with the control monkey on Day 3, indicating release of platelets from the spleen storage pool secondary to PF-0259-related acute thrombocytopenia. Scale bar = 60 µm.</p>

  PublisherDOI

Frequent coauthors

• E. R. G. Eckert

  University of Minnesota System

  187 shared

• W.E. Ibele

  University of Minnesota

  132 shared

• E. M. Sparrow

  University of Minnesota

  60 shared

• E. M. Sparrow

  54 shared

• Suhas V. Patankar

  Innovative Research (United States)

  54 shared

• Colin Scott

  University College Dublin

  45 shared

• Terrence W. Simon

  University of Minnesota

  43 shared

• E. Pfender

  University of Minnesota

  41 shared

Education

• Ph.D., finance

  University of California, Berkeley

  1996

• Ph.D., physics

  University of Illinois, Urbana

Awards & honors

• Smith Breeden Award Nomination for article 'Do Credit Spread…