Vice President of Pathology
Pathology
Dr. Beth L. Thurberg, MD
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Beth Thurberg is an expert in the field of Pathology. She graduated from University of Chicago Pritzker School of Medicine. University of Chicago Pritzker School of Medicine has a rank of 10 in research and a 19 in primary care Beth Thurberg is a published MD. She published 34 publications, including: 'Natural Progression of Canine Glycogen Storage Disease Type IIIa.'
Publications
- α-Galactosidase A Knockout Mice: Progressive Organ Pathology Resembles the Type 2 Later-Onset Phenotype of Fabry Disease.
- Nonclinical safety assessment of recombinant human acid sphingomyelinase (rhASM) for the treatment of acid sphingomyelinase deficiency:the utility of animal models of ...
- Correction of glycogen storage disease type III with rapamycin in a canine model.
- Alglucosidase alfa enzyme replacement therapy as a therapeutic approach for glycogen storage disease type III.
- Adjunctive ?2-agonists reverse neuromuscular involvement in murine Pompe disease.
- Optimization of a histopathological biomarker for sphingomyelin accumulation in Acid sphingomyelinase deficiency.
- ?2 Agonists enhance the efficacy of simultaneous enzyme replacement therapy in murine Pompe disease.
- Histologic abnormalities of placental tissues in Fabry disease: a case report and review of the literature.
- Investigative pathology: leading the post-genomic revolution.
- Later-onset pompe disease: early detection and early treatment initiation enabled by newborn screening.
- Expanding the clinical spectrum of late-onset Pompe disease: Dilated arteriopathy involving the thoracic aorta, a novel vascular phenotype uncovered.
- Biotherapeutic target or sink: analysis of the macrophage mannose receptor tissue distribution in murine models of lysosomal storage diseases.
- Use of direct fluorescence labeling and confocal microscopy to determine the biodistribution of two protein therapeutics, Cerezyme and Ceredase.
- Pompe disease in infants: improving the prognosis by newborn screening and early treatment.
- Long-term monitoring of patients with infantile-onset Pompe disease on enzyme replacement therapy using a urinary glucose tetrasaccharide biomarker.
- Homeostatic role of transforming growth factor-beta in the oral cavity and esophagus of mice and its expression by mast cells in these tissues.
- Cardiac microvascular pathology in Fabry disease: evaluation of endomyocardial biopsies before and after enzyme replacement therapy.
- Pulmonary delivery of recombinant acid sphingomyelinase improves clearance of lysosomal sphingomyelin from the lungs of a murine model of Niemann-Pick disease.
- Evaluation of a low dose, after a standard therapeutic dose, of agalsidase beta during enzyme replacement therapy in patients with Fabry disease.
- Endosialin protein expression and therapeutic target potential in human solid tumors: sarcoma versus carcinoma.
- Temporal neuropathologic and behavioral phenotype of 6neo/6neo Pompe disease mice.
- Optimized preservation of CNS morphology for the identification of glycogen in the Pompe mouse model.
- Differential muscular glycogen clearance after enzyme replacement therapy in a mouse model of Pompe disease.
- Characterization of pre- and post-treatment pathology after enzyme replacement therapy for Pompe disease.
- Chinese hamster ovary cell-derived recombinant human acid alpha-glucosidase in infantile-onset Pompe disease.
- Mice with elevated muscle glycogen stores do not have improved exercise performance.
- Exercise capacity of mice genetically lacking muscle glycogen synthase: in mice, muscle glycogen is not essential for exercise.
- Replacing acid alpha-glucosidase in Pompe disease: recombinant and transgenic enzymes are equipotent, but neither completely clears glycogen from type II muscle fibers.
- High-resolution light microscopy (HRLM) and digital analysis of Pompe disease pathology.
- Conjugation of mannose 6-phosphate-containing oligosaccharides to acid alpha-glucosidase improves the clearance of glycogen in pompe mice.
- Monitoring the 3-year efficacy of enzyme replacement therapy in fabry disease by repeated skin biopsies.
- Globotriaosylceramide accumulation in the Fabry kidney is cleared from multiple cell types after enzyme replacement therapy.
- Natural Progression of Canine Glycogen Storage Disease Type IIIa.
Schools
U Of Chgo Div Of Bio Sci Pritzker Sch Of Med
Brigham and Womens Hospital
Doctors Specialties
- Anatomic Pathology
- Pathology
Accepted Insurances
Education
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Brigham and Women's Hospital -
University of Chicago Pritzker School of Medicine
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