T. Burrow
Professor
Also affiliated: Cincinnati Children's Hospital Medical Center (2006–2018); Arkansas Children's Hospital (2018–2025); University of Miami (2020); Concordia University Irvine (1935); University of Arkansas Medical Center (2020); Lankenau Heart Institute (2017); Science Oxford (1957); Woodlands Hospital (1980); Christ University (1935); University of Cincinnati (2007–2012); University of Newcastle Australia (2012); University of Cincinnati Medical Center (2007–2010)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
T. Burrow's research centers on the diagnosis, management, and progression of various genetic and metabolic disorders, with a particular focus on Gaucher disease and Pompe disease. Burrow has investigated the long-term efficacy and safety of therapeutic interventions for late-onset Pompe disease, including studies on cipaglucosidase alfa in combination with miglustat. Additionally, Burrow's work addresses the complexities of diagnosing and managing glycogen storage disease type IV and Wolman disease, especially in pediatric populations. The researcher has also explored the impact of the COVID-19 pandemic on specific patient communities, such as individuals with Gaucher disease in the US.
Further research interests include mitochondrial ultrastructural defects and the genetic underpinnings of neurodevelopmental disorders, as evidenced by work on NDUFS3-related disorders and variants in the BSN gene. Burrow's scholarship metrics include an h-index of 21, 197 total publications, and 1,262 total citations, with a designation as a highly cited researcher. Collaborations within the University of Arkansas for Medical Sciences include Thomas Andrew Burrow, Carissa Rodriquez, Hannah Barkley, and Ankita Shukla.
Metrics
- h-index: 21
- Publications: 197
- Citations: 1,279
Selected Publications
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Diagnostic Odyssey of Atypical Long‐Chain 3‐Hydroxyacyl‐ <scp>CoA</scp> Dehydrogenase Deficiency ( <scp>LCHADD</scp> ) Explained by Three Allelic Products From Two Pathogenic Variants (2026)
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Central nervous system-symptomatic hyperammonemia following recombinant crisantaspase Pseudomonas fluorescens (2026)
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Longitudinal Observation of Children with Achondroplasia: Findings from a Global Natural History Study (ACHieve) (2026)
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Variants in BSN, encoding the presynaptic protein Bassoon, result in a distinct neurodevelopmental disorder with a broad phenotypic range (2025)
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Correction: Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria (2025)
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Variants in <i>BSN</i> , encoding the presynaptic protein Bassoon, result in a novel neurodevelopmental disorder with a broad phenotypic range (2025)
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Neurodevelopmental delay, musculoskeletal disorders and dysmorphia associated with a novel pathogenic interstitial deletion of chromosome 10q21.1q21.3 (2025)
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Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria (2024)
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04145 Profound hypotonia in a newborn with Biallelic δ-Aminolevulinic Acid Dehydratase (ALAD) mutations (2024)
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Design of a Phase 3 study of AAV-mediated gene transfer of ornithine transcarbamylase (OTC) in patients with late-onset OTC deficiency (2024)
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DESIGN OF A PHASE 3 STUDY OF AAV-MEDIATED GENE TRANSFER OF ORNITHINE TRANSCARBAMYLASE (OTC) IN PATIENTS WITH LATE-ONSET OTC DEFICIENCY (2023)
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Diagnosis and management of glycogen storage disease type IV, including adult polyglucosan body disease: A clinical practice resource (2023)
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Clinical insights from Wolman disease: Evaluating infantile hepatosplenomegaly (2022)
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The diagnosis and management of Gaucher disease in pediatric patients: Where do we go from here? (2022)
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Mitochondrial Ultrastructural Defects in NDUFS3-Related Disorder (2021)
Collaboration Network
Top Collaborators
- The diagnosis and management of Gaucher disease in pediatric patients: Where do we go from here?
- Diagnosis and management of glycogen storage disease type IV, including adult polyglucosan body disease: A clinical practice resource
- Clinical insights from Wolman disease: Evaluating infantile hepatosplenomegaly
- The diagnosis and management of Gaucher disease in pediatric patients: Where do we go from here?
- DESIGN OF A PHASE 3 STUDY OF AAV-MEDIATED GENE TRANSFER OF ORNITHINE TRANSCARBAMYLASE (OTC) IN PATIENTS WITH LATE-ONSET OTC DEFICIENCY
- Design of a Phase 3 study of AAV-mediated gene transfer of ornithine transcarbamylase (OTC) in patients with late-onset OTC deficiency
- Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria
- 04145 Profound hypotonia in a newborn with Biallelic δ-Aminolevulinic Acid Dehydratase (ALAD) mutations
- Correction: Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria
- Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria
- 04145 Profound hypotonia in a newborn with Biallelic δ-Aminolevulinic Acid Dehydratase (ALAD) mutations
- Correction: Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria
- Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria
- 04145 Profound hypotonia in a newborn with Biallelic δ-Aminolevulinic Acid Dehydratase (ALAD) mutations
- Correction: Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria
- Diagnosis and management of glycogen storage disease type IV, including adult polyglucosan body disease: A clinical practice resource
- Clinical insights from Wolman disease: Evaluating infantile hepatosplenomegaly
- DESIGN OF A PHASE 3 STUDY OF AAV-MEDIATED GENE TRANSFER OF ORNITHINE TRANSCARBAMYLASE (OTC) IN PATIENTS WITH LATE-ONSET OTC DEFICIENCY
- Design of a Phase 3 study of AAV-mediated gene transfer of ornithine transcarbamylase (OTC) in patients with late-onset OTC deficiency
- DESIGN OF A PHASE 3 STUDY OF AAV-MEDIATED GENE TRANSFER OF ORNITHINE TRANSCARBAMYLASE (OTC) IN PATIENTS WITH LATE-ONSET OTC DEFICIENCY
- Design of a Phase 3 study of AAV-mediated gene transfer of ornithine transcarbamylase (OTC) in patients with late-onset OTC deficiency
- DESIGN OF A PHASE 3 STUDY OF AAV-MEDIATED GENE TRANSFER OF ORNITHINE TRANSCARBAMYLASE (OTC) IN PATIENTS WITH LATE-ONSET OTC DEFICIENCY
- Design of a Phase 3 study of AAV-mediated gene transfer of ornithine transcarbamylase (OTC) in patients with late-onset OTC deficiency
- DESIGN OF A PHASE 3 STUDY OF AAV-MEDIATED GENE TRANSFER OF ORNITHINE TRANSCARBAMYLASE (OTC) IN PATIENTS WITH LATE-ONSET OTC DEFICIENCY
- Design of a Phase 3 study of AAV-mediated gene transfer of ornithine transcarbamylase (OTC) in patients with late-onset OTC deficiency
- DESIGN OF A PHASE 3 STUDY OF AAV-MEDIATED GENE TRANSFER OF ORNITHINE TRANSCARBAMYLASE (OTC) IN PATIENTS WITH LATE-ONSET OTC DEFICIENCY
- Design of a Phase 3 study of AAV-mediated gene transfer of ornithine transcarbamylase (OTC) in patients with late-onset OTC deficiency
- Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria
- Correction: Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria
- Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria
- Correction: Profound hypotonia in an infant with δ-aminolevulinic acid dehydratase deficient porphyria
- Variants in BSN, encoding the presynaptic protein Bassoon, result in a distinct neurodevelopmental disorder with a broad phenotypic range
- Variants in <i>BSN</i> , encoding the presynaptic protein Bassoon, result in a novel neurodevelopmental disorder with a broad phenotypic range
- Variants in BSN, encoding the presynaptic protein Bassoon, result in a distinct neurodevelopmental disorder with a broad phenotypic range
- Variants in <i>BSN</i> , encoding the presynaptic protein Bassoon, result in a novel neurodevelopmental disorder with a broad phenotypic range
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