About

James D. Murray is Professor Emeritus of Mathematical Biology at the University of Washington. His research interests are in mathematical biology, with a focus on the application of mathematical modelling in medicine, psychology, ecology, epidemiology, and developmental biology. Prior to his position at Washington, he was a Professor of Mathematical Biology and the founding Director of the Centre for Mathematical Biology at the University of Oxford. Professor Murray holds a distinguished academic background with a B.Sc. and Ph.D. in Applied Mathematics from the University of St. Andrews, and an M.A. and Sc.D. from the University of Oxford. His career is marked by numerous honors, including fellowships with the Royal Society (Edinburgh and London), the Institute of Biology, and the European Academy of Sciences. He has received several prestigious awards such as the Naylor Prize for Applied Mathematics, the Bakerian Medal and Prize Lecture from the Royal Society, the IMA Gold Medal, and the William Benter Prize in Applied Mathematics. Murray has held visiting professorships at various institutions worldwide and has been involved in public science communication, including a PBS program and public lectures. His contributions to the field are recognized through his numerous honorary degrees and fellowships, and he has served as President of the European Society for Mathematical & Theoretical Biology. In his personal time, he enjoys medieval art and architecture, as well as 19th-century English watercolour paintings. He resides in New Hope, PA, with his wife, Sheila.

Research topics

• Biology
• Genetics
• Computational biology
• Molecular biology

Selected publications

• M41 High frequency of asymptomatic mediastinal lymph node TB diagnosed via EBUS: a retrospective cohort study from a UK TB-Network

  2025-11-01

  article

  <h3>Introduction</h3> In 2023 extrapulmonary tuberculosis accounted for 62% of TB diagnoses in England, with mediastinal lymph node tuberculosis (MLN-TB) responsible for 14%.¹ MLN-TB symptoms vary, and it may be incidentally detected on chest imaging. Mediastinal lymphadenopathy is now routinely evaluated using endobronchial ultrasound-guided needle aspiration (EBUS-TBNA). We investigated MLN-TB diagnosed with EBUS-TBNA to estimate the frequency of asymptomatic presentations in our TB population. <h3>Methods</h3> We conducted a retrospective study of EBUS-diagnosed MLN-TB in North Central London (NCL) TB Network between 2018–2024. Cases were classified as asymptomatic (no TB-suggestive symptoms, MLN incidentally noticed on imaging) or symptomatic (if typical TB symptoms, or TB-related symptoms led to imaging). A TB diagnostic score was recorded based on the level of evidence contributing to diagnosis, as previously.² <h3>Results</h3> 135 cases were included in the study (table 1): 61 from the Royal Free (RFH), 50 from University College of London (UCLH), and 24 from North Middlesex (NMH) hospital. 49/135 (36%) were identified as asymptomatic MLN-TB, with the remainder symptomatic. Asymptomatic MLN-TB patients were significantly older (mean age 51.2 vs 40.0 years, p=0.002) and more likely to have a history of chronic lung disease (CLD) or cancer than symptomatic individuals. Asymptomatic MLN-TB was more frequently limited to MLN involvement, compared to symptomatic TB (55.1% vs 33.7%, p=0.01). Microbiological confirmation (molecular test or culture) was obtained in similar proportions of asymptomatic and symptomatic individuals (85.7% vs 82.6%) MLN-TB symptoms varied significantly by referral route (p=0.001): inpatient referrals were mostly symptomatic, while two-week wait and other outpatient services captured more asymptomatic cases. <h3>Conclusions</h3> Approximately 36% of our EBUS-diagnosed MLN-TB occurred in asymptomatic individuals having imaging for unrelated indications. Asymptomatic patients were older and more often had prior lung disease or malignancy. Referral route seems to differ according to the clinical presentation of MLN-TB. The growing use of thoracic CT imaging—especially through non-TB-specific pathways—may facilitate incidental detection; mediastinal lymphadenopathy on imaging should prompt consideration of TB and early testing, even in the absence of traditional symptoms and risk factors. <h3>References</h3> UKHSA. Tuberculosis in England, 2024. McNally, <i>et al. Int J Tuberc Lung Dis.</i> 2025;<b>29</b>(5):227–30.

  PublisherDOI

• Determining the impact of an artificial intelligence tool on the management of pulmonary nodules detected incidentally on CT (DOLCE) study protocol: a prospective, non-interventional multicentre UK study

  BMJ Open · 2024-01-01 · 5 citations

  articleOpen access

  INTRODUCTION: In a small percentage of patients, pulmonary nodules found on CT scans are early lung cancers. Lung cancer detected at an early stage has a much better prognosis. The British Thoracic Society guideline on managing pulmonary nodules recommends using multivariable malignancy risk prediction models to assist in management. While these guidelines seem to be effective in clinical practice, recent data suggest that artificial intelligence (AI)-based malignant-nodule prediction solutions might outperform existing models. METHODS AND ANALYSIS: This study is a prospective, observational multicentre study to assess the clinical utility of an AI-assisted CT-based lung cancer prediction tool (LCP) for managing incidental solid and part solid pulmonary nodule patients vs standard care. Two thousand patients will be recruited from 12 different UK hospitals. The primary outcome is the difference between standard care and LCP-guided care in terms of the rate of benign nodules and patients with cancer discharged straight after the assessment of the baseline CT scan. Secondary outcomes investigate adherence to clinical guidelines, other measures of changes to clinical management, patient outcomes and cost-effectiveness. ETHICS AND DISSEMINATION: This study has been reviewed and given a favourable opinion by the South Central-Oxford C Research Ethics Committee in UK (REC reference number: 22/SC/0142).Study results will be available publicly following peer-reviewed publication in open-access journals. A patient and public involvement group workshop is planned before the study results are available to discuss best methods to disseminate the results. Study results will also be fed back to participating organisations to inform training and procurement activities. TRIAL REGISTRATION NUMBER: NCT05389774.

  PublisherOA PDFDOI

• Regulatorische Dysfunktion hemmt die Entwicklung und Anwendung von transgenen Nutztieren in der Landwirtschaft

  2023-01-01

  book-chapter1st authorCorresponding
  PublisherDOI

• Salmonella enhances osteogenic differentiation in adipose-derived mesenchymal stem cells

  Frontiers in Cell and Developmental Biology · 2023-03-15 · 6 citations

  articleOpen accessCorresponding

  The potential of mesenchymal stem cells (MSCs) for tissue repair and regeneration has garnered great attention. While MSCs are likely to interact with microbes at sites of tissue damage and inflammation, like in the gastrointestinal system, the consequences of pathogenic association on MSC activities have yet to be elucidated. This study investigated the effects of pathogenic interaction on MSC trilineage differentiation paths and mechanisms using model intracellular pathogen Salmonella enterica ssp enterica serotype Typhimurium. The examination of key markers of differentiation, apoptosis, and immunomodulation demonstrated that Salmonella altered osteogenic and chondrogenic differentiation pathways in human and goat adipose-derived MSCs. Anti-apoptotic and pro-proliferative responses were also significantly upregulated ( p &amp;lt; 0.05) in MSCs during Salmonella challenge. These results together indicate that Salmonella , and potentially other pathogenic bacteria, can induce pathways that influence both apoptotic response and functional differentiation trajectories in MSCs, highlighting that microbes have a potentially significant role as influencers of MSC physiology and immune activity.

  PublisherOA PDFDOI

• MSC therapy in livestock models

  Translational Animal Science · 2022-01-01 · 14 citations

  reviewOpen accessSenior authorCorresponding

  Mesenchymal stem cells (MSCs) have great value as therapeutic tools in a wide array of applications in regenerative medicine. The wide repertoire of cell functions regarding tissue regeneration, immunomodulation, and antimicrobial activity makes MSC-based therapy a strong candidate for treatment options in a variety of clinical conditions and should be studied to expand the current breadth of knowledge surrounding their physiological properties and therapeutic benefits. Livestock models are an appropriate resource for testing the efficacy of MSC therapies for their use in biomedical research and can be used to improve both human health and animal agriculture. Agricultural animal models such as pigs, cattle, sheep, and goats have grown in popularity for in vivo research relative to small animal models due to their overlapping similarities in structure and function that more closely mimic the human body. Cutaneous wound healing, bone regeneration, osteoarthritis, ischemic reperfusion injury, and mastitis recovery represent a few examples of the types of disease states that may be investigated in livestock using MSC-based therapy. Although the cost of agricultural animals is greater than small animal models, the information gained using livestock as a model holds great value for human applications, and in some cases, outcompetes the weight of information gained from rodent models. With emerging fields such as exosome-based therapy, proper in vivo models will be needed for testing efficacy and translational practice, i.e., livestock models should be strongly considered as candidates. The potential for capitalizing on areas that have crossover benefits for both agricultural economic gain and improved health of the animals while minimizing the gap between translational research and clinical practice are what make livestock great choices for experimental MSC models.

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• A deletion at the polled PC locus alone is not sufficient to cause a polled phenotype in cattle

  Scientific Reports · 2022-02-08 · 8 citations

  articleOpen accessSenior author

  allele) comprised of a 212 bp duplicated DNA sequence replacing a 10-bp sequence at the polled locus is associated with the hornless phenotype (polled) in cattle. To test the hypothesis that the 10 bp deletion alone is sufficient to result in polled, a CRISPR-Cas9 dual guide RNA approach was optimized to delete a 133 bp region including the 10 bp sequence. Timing of ribonucleoprotein complex injections at various hours post insemination (hpi) (6, 8, and 18 hpi) as well as in vitro transcribed (IVT) vs synthetic gRNAs were compared. Embryos injected 6 hpi had a significantly higher deletion rate (53%) compared to those injected 8 (12%) and 18 hpi (7%), and synthetic gRNAs had a significantly higher deletion rate (84%) compared to IVT gRNAs (53%). Embryo transfers were performed, and bovine fetuses were harvested between 3 and 5 months of gestation. All fetuses had mutations at the target site, with two of the seven having biallelic deletions, and yet they displayed horn bud development indicating that the 10 bp deletion alone is not sufficient to result in the polled phenotype.

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• LincRNA#1 knockout alone does not affect polled phenotype in cattle heterozygous for the celtic POLLED allele

  Scientific Reports · 2022-05-10 · 3 citations

  articleOpen accessSenior author

  Abstract A long intergenic non-coding RNA ( lincRNA#1 ) is overexpressed in the horn bud region of polled (hornless) bovine fetuses, suggesting a potential role in horn bud suppression. Genome editing was used to test whether the absence of this sequence was associated with the horned phenotype. Two gRNAs with high mutation efficiencies targeting the 5′ and the 3′ regions flanking the lincRNA#1 sequence were co-injected with Cas9 as ribonucleoprotein complexes into bovine zygotes (n = 121) 6 h post insemination. Of the resulting blastocysts (n = 31), 84% had the expected 3.7 kb deletion; of these embryos with the 3.7 kb deletions, 88% were biallelic knockouts. Thirty-nine presumptive edited 7-day blastocysts were transferred to 13 synchronized recipient cows resulting in ten pregnancies, five with embryos heterozygous for the dominant P C POLLED allele at the POLLED locus, and five with the recessive pp genotype. Eight (80%) of the resulting fetuses were biallelic lincRNA#1 knockouts, with the remaining two being mosaic. RT-qPCR analysis was used to confirm the absence of lincRNA#1 expression in knockout fetuses. Phenotypic and histological analysis of the genotypically (P C p) POLLED , lincRNA#1 knockout fetuses revealed similar morphology to non-edited, control polled fetuses, indicating the absence of lincRNA#1 alone does not result in a horned phenotype.

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• One-step generation of a targeted knock-in calf using the CRISPR-Cas9 system in bovine zygotes

  BMC Genomics · 2021 · 35 citations

  • Biology
  • Genetics
  • Molecular biology

  BACKGROUND: The homologous recombination (HR) pathway is largely inactive in early embryos prior to the first cell division, making it difficult to achieve targeted gene knock-ins. The homology-mediated end joining (HMEJ)-based strategy has been shown to increase knock-in efficiency relative to HR, non-homologous end joining (NHEJ), and microhomology-mediated end joining (MMEJ) strategies in non-dividing cells. RESULTS: By introducing gRNA/Cas9 ribonucleoprotein complex and a HMEJ-based donor template with 1 kb homology arms flanked by the H11 safe harbor locus gRNA target site, knock-in rates of 40% of a 5.1 kb bovine sex-determining region Y (SRY)-green fluorescent protein (GFP) template were achieved in Bos taurus zygotes. Embryos that developed to the blastocyst stage were screened for GFP, and nine were transferred to recipient cows resulting in a live phenotypically normal bull calf. Genomic analyses revealed no wildtype sequence at the H11 target site, but rather a 26 bp insertion allele, and a complex 38 kb knock-in allele with seven copies of the SRY-GFP template and a single copy of the donor plasmid backbone. An additional minor 18 kb allele was detected that looks to be a derivative of the 38 kb allele resulting from the deletion of an inverted repeat of four copies of the SRY-GFP template. CONCLUSION: The allelic heterogeneity in this biallelic knock-in calf appears to have resulted from a combination of homology directed repair, homology independent targeted insertion by blunt-end ligation, NHEJ, and rearrangement following editing of the gRNA target site in the donor template. This study illustrates the potential to produce targeted gene knock-in animals by direct cytoplasmic injection of bovine embryos with gRNA/Cas9, although further optimization is required to ensure a precise single-copy gene integration event.

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• Harnessing endogenous repair mechanisms for targeted gene knock-in of bovine embryos

  Scientific Reports · 2020 · 7 citations

  • Biology
  • Genetics
  • Computational biology

  Introducing useful traits into livestock breeding programs through gene knock-ins has proven challenging. Typically, targeted insertions have been performed in cell lines, followed by somatic cell nuclear transfer cloning, which can be inefficient. An alternative is to introduce genome editing reagents and a homologous recombination (HR) donor template into embryos to trigger homology directed repair (HDR). However, the HR pathway is primarily restricted to actively dividing cells (S/G2-phase) and its efficiency for the introduction of large DNA sequences in zygotes is low. The homology-mediated end joining (HMEJ) approach has been shown to improve knock-in efficiency in non-dividing cells and to harness HDR after direct injection of embryos. The knock-in efficiency for a 1.8 kb gene was contrasted when combining microinjection of a gRNA/Cas9 ribonucleoprotein complex with a traditional HR donor template or an HMEJ template in bovine zygotes. The HMEJ template resulted in a significantly higher rate of gene knock-in as compared to the HR template (37.0% and 13.8%; P < 0.05). Additionally, more than a third of the knock-in embryos (36.9%) were non-mosaic. This approach will facilitate the one-step introduction of gene constructs at a specific location of the bovine genome and contribute to the next generation of elite cattle.

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• PSX-32 Late-Breaking Abstract: Production of a Gene Knock-In Bull Calf by Embryo-Mediated Genome Editing

  Journal of Animal Science · 2020-11-03 · 1 citations

  articleOpen access

  Abstract Genome editing offers an opportunity to introduce targeted gene insertions into livestock breeding programs. Molecular geneticists have typically employed a donor repair template and the homologous recombination (HR) pathway in somatic cells to introduce gene knock-ins into livestock genomes, followed by cloning. Editing embryos directly to achieve targeted gene knock-ins is inefficient, especially for introducing large DNA sequences. Here we report using a one-step method to produce a gene knock-in bull calf by cytoplasmic microinjection of CRISPR/Cas9 reagents into a bovine embryo. In vitro fertilized one-cell bovine zygotes were injected with a gRNA/Cas9 ribonucleoprotein complex and homology mediated end joining donor template containing the sex determining region Y (SRY) gene, the green fluorescent protein (gfp) reporter gene driven by the SV40 promoter, and one kilobase homology arms targeting the H11 safe harbor locus on bovine chromosome 17. Seven-day blastocysts were evaluated using fluorescent microscopy, and nine green fluorescent embryos were transferred to synchronized recipients. Ultrasound evaluation at 35 days revealed one pregnancy. In April 2020, a healthy 50 kg male calf was born. DNA was extracted from placenta, blood and a fibroblast line derived from the calf and analyzed for SRY-GFP knock-in, as well as genotypic sex. PCR and Sanger sequencing revealed the biallelic edit of the target location on chromosome 17, with the insertion of three or seven copies of the SRY-GFP construct in addition to donor plasmid backbone, or a 26 base pair insertion, and an XY genotype. Future analysis of the XX offspring inheriting the SRY gene on chromosome 17 from this knock-in bull will reveal whether inheritance of the bovine SRY gene is sufficient to trigger the male developmental pathway in cattle.

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Frequent coauthors

• Elizabeth A. Maga

  University of California, Davis

  47 shared

• A. T. Bowling

  22 shared

• Douglas F. Antczak

  Cornell University

  20 shared

• Pablo J. Ross

  STgenetics (United States)

  19 shared

• T. J. Hopman

  Cornell University

  17 shared

• Alexandre Rodrigues Caetano

  Brazilian Agricultural Research Corporation

  17 shared

• Jason Lin

  Chiba Cancer Center

  16 shared

• Sadie L. Hennig

  University of California, Davis

  16 shared

Education

• Other

  University of St. Andrews

  1994

• Other

  University of Strathclyde

  1999

• Other

  University of Milan

  2004

• Other

  University of Waterloo

  2006

• Other

  University of Dundee

  2011

Awards & honors

• Guggenheim Fellow 1968
• Fellow of the Royal Society (Edinburgh) 1979
• Ulam Visiting Scholar, Los Alamos National Laboratory 1985
• Fellow of the Royal Society (London) 1985
• Fellow of the Institute of Biology (Great Britain) 1988