Julie Wilhelmy

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Julie Wilhelmy, is a Life Science Research Assistant at the Stanford Genome Technology Center, Department of Biochemistry, School of Medicine, Stanford University, Stanford, CA and a research team member at the ME/CFS Collaborative Research Center at Stanford.[1] Her research interests include experimental genomics and immunology. Projects include: analyzing the gene expression patterns of the severely ill patients; analysis of T Cell receptors and gene expression of single cells in Mark Davis' lab; Metabolic Trap Project with Robert Phair; and energy metabolism of ME/CFS patient immune cells with Layla Cervantes.[2]

Research related to ME/CFS[edit | edit source]

  • Feb 2019, Red blood cell deformability is diminished in patients with Chronic Fatigue Syndrome[3] - (Full text)
  • Apr 2019, A nanoelectronics-blood-based diagnostic biomarker for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)[4] - (Full text)

See also[edit | edit source]

Learn more[edit | edit source]

References[edit | edit source]

  1. "SGTC :: Staff". www-sequence.stanford.edu. Retrieved June 10, 2019.
  2. "Meet Julie Wilhelmy, ME/CFS Collaborative Research Center at Stanford Team Member". Open Medicine Foundation. July 25, 2018. Retrieved June 10, 2019.
  3. Saha, Amit K.; Schmidt, Brendan R.; Wilhelmy, Julie; Nguyen, Vy; Abugherir, Abed; Do, Justin K.; Nemat-Gorgani, Mohsen; Davis, Ronald W.; Ramasubramanian, Anand K. (February 23, 2019). "Red blood cell deformability is diminished in patients with Chronic Fatigue Syndrome". Clinical Hemorheology and Microcirculation. 71 (1): 113–116. doi:10.3233/CH-180469.
  4. Esfandyarpour, R.; Kashi, A.; Nemat-Gorgani, M.; Wilhelmy, J.; Davis, R. W. (May 21, 2019). "A nanoelectronics-blood-based diagnostic biomarker for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)". Proceedings of the National Academy of Sciences. 116 (21): 10250–10257. doi:10.1073/pnas.1901274116. ISSN 0027-8424.

genome an organism's complete set of DNA, including all of its genes

metabolic trap hypothesis An hypothesis which proposes that the normal metabolic functioning of the cell has become "trapped" in an abnormal state, which may lead to body-wide symptoms.

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From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history.