The ME/CFS and control sample sizes in this study provided greater than 90% power, with 0

The ME/CFS and control sample sizes in this study provided greater than 90% power, with 0.05, to detect the same frequencies of antibody reactivity previously observed in the PTLDS patients and associated controls (Chandra et al., 2010). 51 ME/CFS patients (36 female; mean [SD] age, 51.2 [11.7] years) and 53 age- and gender-matched healthy controls (40 female; mean age, 50.0 [13.6] years), provided by the SolveCFS BioBank (Irlbeck et al., 2014). This study was approved by the Institutional Review Board of Columbia University Medical Center. The ME/CFS and control sample sizes in this study provided greater than 90% power, with 0.05, to detect the same frequencies of antibody reactivity previously observed in the PTLDS patients and associated controls (Chandra et al., 2010). ME/CFS patients met the Fukuda or the Canadian criteria for this condition (Carruthers, 2007; Fukuda et al., 1994) and Gpr20 lacked histories suggestive of Lyme disease. Screening questionnaires were used to evaluate the general health of the unaffected controls and to confirm that that they did not meet ME/CFS case definition criteria. In contrast to the findings of Azoxymethane our prior study on PTLDS patients (Chandra et al., 2010), we found no significant difference Azoxymethane in the prevalence of anti-neural antibody reactivity between ME/CFS patients (4 of 51; 7.8%) and healthy controls (7 of 53; 13.2%) ( em p /em =0.5). Although often detectable (Chandra et al., 2010), it is unclear whether the presence of anti-neural antibodies has a role in the pathogenesis of certain PTLDS manifestations. If these antibodies do play a role, it would appear that the cause of the Azoxymethane somewhat similar symptoms in ME/CFS is different. A potential limitation of the methodology employed in this and in our prior study (Chandra et al., 2010) is that it primarily detects reactivity to prominently expressed neural proteins and can miss reactivity to some minor proteins or non-protein antigens. Further inquiry into B cell activation mechanisms and autoantibody response Azoxymethane may be useful to gaining a better understanding of differences between PTLDS and ME/CFS, and might provide potential markers for the identification of disease subsets. Acknowledgments Funding/support: Research reported here was supported by grants from the Solve ME/CFS Initiative, the National Institute of Allergy and Infectious Diseases of the National Institutes of Health (R56AI093763 and R21AI071180), and the Lyme Research Alliance. The funding organizations had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Disclaimer and potential conflicts of interest: Dr. Alaedini reports receiving grants from the National Azoxymethane Institutes of Health and the Lyme Research Alliance for research related to Lyme disease, and from the Solve ME/CFS Initiative for research related to ME/CFS. Dr. Wormser reports receiving research grants from Immunetics, Inc., Rarecyte, Inc., Institute for Systems Biology, and bioMrieux SA. He owns equity in Abbott; has been an expert witness in malpractice cases involving Lyme disease and babesiosis; is an unpaid board member of the American Lyme Disease Foundation; and was a consultant to Baxter for Lyme disease vaccine development..