David Nelson
VerifiedUniversity of Minnesota · Molecular and Cellular Biology
Active 1850–2026
About
David Nelson is the Arthur K. Solomon Professor of Biophysics and a Professor of Physics and Applied Physics at Harvard University within the Department of Molecular & Cellular Biology. His research focuses on problems that bridge the physical and biological sciences. Early in his career, he explored population dynamics in environments with varying growth rates and convection, leading to universal predictions for the spreading and transverse profile of populations in space- and time-dependent environments. He developed a theory of force-induced denaturation of double-stranded DNA with his student, David Lubensky, which examines how sequence heterogeneity influences the dynamics of DNA unzipping and the implications for DNA replication. His recent work includes observations of jumps and plateaus in the unzipping of lambda phage DNA under constant force, consistent with his theoretical predictions. Nelson has also studied the effects of sequence heterogeneity on motor proteins such as helicases, exonucleases, and RNA polymerases, providing insights into their velocity-force relationships near stall forces. Additionally, he has investigated the shapes of viruses, demonstrating that the icosahedral packing of protein capsomeres becomes unstable to faceting as virus size increases, and developed a parametrization of virus shell architecture using a dimensionless 'von Karman number' to explain why small viruses are round and large ones are faceted.
Research topics
- Political Science
- Medicine
- Computer Science
- Pathology
- Psychology
- Medical education
- History
- Internal medicine
- Surgery
- Geography
- Virology
- Public relations
- Clinical psychology
- Psychiatry
Selected publications
Research Square · 2026-04-23
preprintOpen access1st authorCorrespondingbioRxiv (Cold Spring Harbor Laboratory) · 2026-03-18
articleOpen access. Midgestation is a period of rapid growth for placenta and embryo, yet it remains unclear how the placental tissues expand without directly competing with the embryo for biosynthetic resources. Here, we show that this midgestational metabolic transition is associated with a marked reduction in embryonic expression of purine salvage enzymes, which constrains embryonic metabolism and leads to different strategies for purine synthesis between the placenta and embryo. Midgestation embryos are unable to engage the purine salvage pathway even when de novo purine synthesis is blocked either in vivo or in ex utero embryo culture, whereas placental tissue and trophoblasts retain the capacity to use either pathway. Disruption of de novo purine synthesis in mice causes reduced embryonic growth, impaired axial elongation, and abnormal brain and placental development, which are only partially rescued by supplementation with purine salvage precursors. In human placenta, trophoblast stem cells readily switch between the de novo and salvage pathways based on nutrient availability, and syncytiotrophoblasts (STB) preferentially rely on the salvage pathway. We identified guanosine monophosphate (GMP) as a metabolic checkpoint regulating STB differentiation, with insufficient GMP levels causing degradation of the small GTPase Rheb and failure of mTOR activation. Supplementation of purine salvage substrates restored GMP synthesis and STB differentiation in humans, but not mice. Further, in vivo measurements in humans revealed that maternal circulating hypoxanthine decreases during pregnancy and is further reduced in women with clinically small placentas, highlighting the role of hypoxanthine in supporting placental growth. These results uncover compartmentalized purine salvage between the embryo and placenta as a mechanism that limits competition for biosynthetic resources and enables coordinated growth during mammalian development.
Journal of Thoracic and Cardiovascular Surgery · 2026-04-24
articleSenior authorPhysiology · 2026-05-01
articleBackground: Hypertensive disorders of pregnancy (HDP) are marked by excessive inflammatory responses and dysregulation of angiogenic factors that contribute to maladaptive placentation. While studies have investigated inflammation or angiogenic factors in HDP, few have included longitudinal and broad simultaneous assessment of these biomarkers. Thus, we studied the hypothesis that women who developed an HDP would express a greater pro-inflammatory profile and dysregulation of angiogenic factors from early-to-late gestation, whereby these outcomes would be related. Methods: Eleven women with normal pregnancies (NORM; age: 30±6 y; body mass index [BMI]: 27.3±7.6 kg/m 2 ) and 9 women who developed HDP (age: 32±4 y; BMI: 27.7±5.3 kg/m 2 ) were studied during early (4-12 weeks) and late (30-34 weeks) gestation. Serum and plasma samples were taken at each visit. Pro-angiogenic (placental growth factor [PlGF]) and anti-angiogenic (soluble endoglin [sENG], soluble fms-like tyrosine kinase-1 [sFlt-1]) factors were measured using ELISA. Corin, an enzyme indirectly affecting vascular remodeling, was also measured via ELISA. Pro-inflammatory (IFN-γ, IL-1β, IL-2, IL-6, IL-8, IL-12p70, IL-17A, IP-10, MCP-1, and TNF-α) and anti-inflammatory (IL-4, IL-10) cytokines were measured using a multiplex bead-based immunoassay. Cytokine data are reported as geometric mean ± geometric SD factor, while all other data are arithmetic mean ± SD. Results: Regarding pro-angiogenic factors, PlGF increased from early-to-late pregnancy (NORM: 37.4±35.0 to 294.2±252.2 pg/mL; HDP: 30.1±14.7 to 166.5±14.3 pg/mL; time P < 0.001). For anti-angiogenic factors, sENG increased from early-to-late pregnancy (NORM: 4.87±1.07 to 6.30±3.18 ng/mL; HDP: 6.32±1.17 to 10.07±3.05 ng/mL; time P < 0.001), was greater in HDP (group P = 0.006), and trended towards an interaction (P = 0.086). sFlt-1 tended to increase across pregnancy (NORM: 7135±2891 to 10468±10588 pg/mL; HDP: 7282±2620 to 11928±7429 pg/mL; time P = 0.051). Further, corin increased while sFlt-1:PlGF ratio decreased across pregnancy (both P ≤ 0.002), with corin trending towards an interaction (P = 0.083). Regarding pro-inflammatory cytokines, HDP expressed lower IL-2 (P = 0.004; group effect) and interactions were noted for IL-8 and MCP-1 (both P ≤ 0.037). Both cytokine concentrations decreased across pregnancy in NORM (IL-8: 9.16±7.10 to 4.99±6.90 pg/mL; MCP-1: 90.08±2.24 to 53.32±1.97 pg/mL; both P ≤ 0.002) but not in HDP (IL-8: 13.24±8.08 to 12.43±7.38 pg/mL; MCP-1: 115.34±2.48 to 120.82±2.63 pg/mL; both P ≥ 0.766). For anti-inflammatory cytokines, an interaction was noted for IL-4 (P = 0.022) with a reduction from early-to-late in NORM (5.96±1.63 to 4.13±1.84 pg/mL; P = 0.030), but not HDP (4.88±4.54 to 6.36±5.45 pg/mL; P = 0.184). No other interactions were noted for other cytokines (P range: 0.146-0.759). The early-to-late change (Δ) in sFlt-1 related to ΔIL-17A (r = 0.535; P = 0.033), ΔIL-10 (r = 0.506; P = 0.046), and ΔIL-12p70 (r = 0.632; P = 0.012). Additionally, Δcorin related to ΔIP-10 (r = 0.719; P = 0.013) and ΔsFlt-1:PlGF ratio correlated with ΔIL-6 (r = 0.744; P = 0.004). Conclusions: Our findings demonstrate that the inflammatory profile changes exhibited in women during normal pregnancy are not mirrored in women who develop HDP. Importantly, while we did not observe significant group-by-time interactions in angiogenic factors, several inflammatory cytokines were moderately-to-strongly correlated with these biomarkers. Taken together, these preliminary data suggest that dysregulation of the angiogenic factors promoting proper placentation may contribute to a greater late pregnancy inflammatory load and the development of HDP. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Journal of Primary Care & Community Health · 2026-05-01
articleOpen accessIntroduction/ObjectivesSDOH screening is increasingly required, yet is often operationalized as EHR documentation. The objective of this project was to explore how social workers and nurse case managers experience SDOH screening and how care settings shape its meaning and practice.MethodsWe conducted semi-structured interviews with 10 staff members (6 social workers, 4 nurse case managers) across inpatient and outpatient follow-up contexts in a large academic health system and analyzed transcripts using Colaizzi's phenomenological method.ResultsFive themes emerged: negotiating patient autonomy, conversational personalization, technological and systemic frustrations, staff expertise, and interprofessional collaboration. Participants reported time pressure, emotional labor, and moral distress when needs were identified without reliable pathways to assistance, and they described contrasting inpatient urgency and outpatient continuity that influenced disclosure, trust, and follow-up.ConclusionsSDOH screening was experienced as relationship-centered work that depends on supportive workflows and response capacity; implementation should pair screening mandates with training, streamlined documentation, and closed-loop referral processes.
American Heart Journal · 2026-01-25
articleOpen accessBACKGROUND: Electrical storm (ES) is a clinical syndrome characterized by densely clustered ventricular arrhythmias and associated with substantial morbidity and mortality. Autonomic dysfunction is thought to play key role in the pathophysiology of ES, with sympathetic blockade considered a therapeutic target. However, robust data supporting this treatment strategy remain limited. The objective of the SEDATE trial is to evaluate the effectiveness and safety of dexmedetomidine in the acute management of ES. METHODS AND DESIGN: SEDATE is a multicenter, double-blinded, randomized trial comparing dexmedetomidine to placebo in the acute treatment of patients with ES. A total of 192 participants admitted to an intensive care unit with ES will be randomized in a 1:1 fashion to receive either dexmedetomidine or placebo. Participants will undergo a study drug titration phase, followed by a 48-hour maintenance period and a subsequent study drug weaning phase. The primary outcome is a composite of all-cause in-hospital mortality and/or recurrent ventricular arrhythmia prompting intervention. All participants will be followed for the duration of their hospitalization. IMPLICATION: The SEDATE clinical trial aims to determine whether early use of dexmedetomidine improves in-hospital outcomes in patients with ES. TRIAL REGISTRATION: clinicaltrials.gov NCT06281977.
Inmate Mental Health Assistants
Cambridge University Press eBooks · 2026-04-29
book-chapterAnalysis of Hysterotomy Extension at Unscheduled Cesarean Delivery
American Journal of Perinatology · 2025-05-06 · 1 citations
articleAbstract This study aimed to determine if the rate of hysterotomy extensions increases with increasing cervical dilation in unscheduled cesarean deliveries, and to develop a measure of the severity of hysterotomy extension for quantifying morbidity. This is a retrospective study of unscheduled cesarean deliveries relating to labor dystocia and/or nonreassuring tracings from January 1, 2021, to December 31, 2021. Severe extension was defined as bilateral or adjacent to a structure such as the uterine artery, broad ligament, or cervix, and was compared with uterine artery extensions alone. There were 990 unscheduled cesarean deliveries included. Extensions (n = 233) significantly increased with increasing cervical dilation (p < 0.0001), complicating more than 30 and 50% at 6 and 10 cm of cervical dilation, respectively. Apart from this trend, a logistic regression analysis indicated cervical dilation was an independent risk factor for extension. Transfusions of at least 2 units of blood were five times (26 vs. 5%) more likely for patients with severe extensions than no extension (p < 0.0001). Hysterotomy extensions significantly increase with increasing cervical dilation, and cervical dilation is an independent risk factor for extension. A composite measure of severity accounts for different types of extension when quantifying morbidity, but uterine artery extension is the primary driver of maternal morbidity in cases without hysterectomy.
2025-12-17
reportWhole Blood in the Management of Postpartum Hemorrhage
O&G Open · 2025-10-01
articleOpen accessSenior authorWhole blood (WB) has been shown to improve outcomes in military acute trauma patients and, to a limited extent, in civilian trauma and acute obstetric hemorrhage. The objective of this study was to examine maternal outcomes in patients receiving WB compared with component therapy (defined as packed red blood cells with plasma) for postpartum hemorrhage (PPH). Fifty-two patients met inclusion criteria. The WB group required fewer total blood products, intravenous fluids, and repeated operative procedures. This report demonstrates the potential benefit for use of WB in cases of acute PPH.
Recent grants
NIH · $7.2M · 2007
NIH · $2.4M · 2004
Frequent coauthors
- 148 shared
Jeffrey P. Louie
University of Minnesota Children's Hospital
- 148 shared
Jennifer L. Trainor
Northwestern University
- 148 shared
Richard Malley
Boston Children's Hospital
- 148 shared
Ian McCaslin
Tulane University
- 148 shared
Mark G. Roback
University of Colorado Denver
- 148 shared
Francine Kaufman
- 146 shared
Kimberly S. Quayle
- 146 shared
Nathan Kuppermann
University of California, Davis
Labs
Education
- 1980
Ph.D., Biophysics
Harvard University
- 1975
B.S., Physics
University of California, San Diego
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