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Faculty
Faculty

James G Taylor

Director

  • Center For Sickle Cell Disease
  • College of Medicine
  • Professor
    Internal Medicine
  • Professor
    Microbiology

Education & Expertise

Education

medicine

M.D.
Medical College of Wisconsin
1995

Pediatrics

Residency
Washington University, St. Louis
1998

Pediatric Hematology/Oncology

Fellowship
Johns Hopkins University School of Medicine/NIH
2001

human genetics research

post-doctoral fellowship
National Cancer Institute
2004

Expertise

Hematology, sickle cell disease, genetics and genomics

Academics

Academics

Molecules and Cells course (M1)

Hematology/Medical Oncology Fellowship Program

Thalassemias; Hemoglobinopathies; Adult Acute Lymphoblastic Leukemia; Myelodysplastic Syndromes; Non-malignant Hematology Board Review

Research

Research

Specialty

Disease specific research - sickle cell disease

Funding

  1. P50 HL118006, NHLBI/NIH:  Center for Hemoglobin Research in Minorities (CHarM)

          Taylor, Robert E. (PI)

          Role: Co-Investigator

         10% effort (2017)

 

  1. Faculty start-up Award (2017-2019): Howard University College of Medicine (Medicine) and Center for Sickle Cell Disease

          Translational analysis of mechanisms of pain in sickle cell disease

          Role: PI

 

  1. Pfizer

          RESET clinical trial

          Role: PI

Accomplishments

Accomplishments

2023 John Benjamin Nichols Award

Featured News

Published Articles and Presentations

Published Articles and Presentations

Antiviral response and HIV-1 inhibition in sickle cell disease

https://www.cell.com/iscience/fulltext/S2589-0042(24)00034-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2589004224000348%3Fshowall%3Dtrue

Sickle cell disease (SCD) is characterized by hemolysis, vaso-occlusion, and ischemia. HIV-1 infection was previously shown to be suppressed in SCD PBMCs. Here, we report that HIV-1 suppression is attributed to the increased expression of iron, hypoxia, and interferon-induced innate antiviral factors.

Soluble urokinase-type plasminogen activator receptor in sickle cell disease–associated chronic kidney disease

https://ashpublications.org/bloodadvances/article/7/9/1854/486589/Soluble-urokinase-type-plasminogen-activator

Renal manifestations are the most common complications of sickle cell disease (SCD). Renal disease starts during childhood and progresses further in adults.1 Approximately 30% of patients with SCD develop chronic kidney disease (CKD), and 14% to 18% of them progress to end-stage kidney disease. Thus, there is an urgent need to find specific biomarkers for the early detection of CKD in patients with SCD.

Routine Screening for Sickle Cell Disease during Pregnancy: Epidemiological and Haemoglobin Profile in Congo

https://pubmed.ncbi.nlm.nih.gov/35928545/

Sickle-cell disease, a genetic condition with a high prevalence in sub-Saharan Africa, is transmitted in an autosomal recessive mode. Its screening during pregnancy makes it possible to identify carriers of the S gene which constitute a risk for the unborn child. In order to promote the use of immuno-chromatographic tests, we have set ourselves the task of establishing the epidemiological profile and determining the Emmel test performance.

The gut microbiome in sickle cell disease: Characterization and potential implications

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0255956

Sickle Cell Disease (SCD) is an inherited blood disorder that leads to hemolytic anemia, pain, organ damage and early mortality. It is characterized by polymerized deoxygenated hemoglobin, rigid sickle red blood cells and vaso-occlusive crises (VOC). Recurrent hypoxia-reperfusion injury in the gut of SCD patients could increase tissue injury, permeability, and bacterial translocation. In this context, the gut microbiome, a major player in health and disease, might have significant impact. This study sought to characterize the gut microbiome in SCD.

Association between plasma and urinary orosomucoid and chronic kidney disease in adults with sickle cell disease

https://onlinelibrary.wiley.com/doi/10.1111/bjh.16702

Chronic kidney disease (CKD) strongly contributes to morbidity and mortality in ageing sickle cell disease (SCD) patients.1 Biomarkers for early stage CKD, such as proteinuria, microalbuminuria and reduced glomerular filtration rate (GFR), are difficult to detect in SCD patients because of a urine concentration defect. Thus, new biomarkers, which reflect the unique renal pathology of SCA-associated CKD, are needed for early detection and treatment.